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  • 1.
    Berhan, Yonas
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Eliasson, Mats
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Möllsten, Anna
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Waernbaum, Ingeborg
    Umeå University, Faculty of Social Sciences, Umeå School of Business and Economics (USBE), Statistics.
    Dahlquist, Gisela
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Impact of Parental Socioeconomic Status on Excess Mortality in a Population-Based Cohort of Subjects With Childhood-Onset Type 1 Diabetes2015In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 38, no 5, p. 827-832Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: The aim of this study was to analyze the possible impact of parental and individual socioeconomic status (SES) on all-cause mortality in a population-based cohort of patients with childhood-onset type 1 diabetes.

    RESEARCH DESIGN AND METHODS: Subjects recorded in the Swedish Childhood Diabetes Registry (SCDR) from 1 January 1978 to 31 December 2008 were included (n =14,647). The SCDR was linked to the Swedish Cause of Death Registry (CDR) and the Longitudinal Integration Database for Health Insurance and Labour Market Studies (LISA).

    RESULTS: At a mean follow-up of 23.9 years (maximum 46.5 years), 238 deaths occurred in a total of 349,762 person-years at risk. In crude analyses, low maternal education predicted mortality for male patients only (P = 0.046), whereas parental income support predicted mortality in both sexes (P < 0.001 for both). In Cox models stratified by age-at-death group and adjusted for age at onset and sex, parental income support predicted mortality among young adults (≥18 years of age) but not for children. Including the adult patient’s own SES in a Cox model showed that individual income support to the patient predicted mortality occurring at ≥24 years of age when adjusting for age at onset, sex, and parental SES.

    CONCLUSIONS: Exposure to low SES, mirrored by the need for income support, increases mortality risk in patients with childhood-onset type 1 diabetes who died after the age of 18 years.

  • 2. Brand, Judith S.
    et al.
    van der Schouw, Yvonne T.
    Onland-Moret, N. Charlotte
    Sharp, Stephen J.
    Ong, Ken K.
    Khaw, Kay-Tee
    Ardanaz, Eva
    Amiano, Pilar
    Boeing, Heiner
    Chirlaque, Maria-Dolores
    Clavel-Chapelon, Francoise
    Crowe, Francesca L.
    de Lauzon-Guillain, Blandine
    Duell, Eric J.
    Fagherazzi, Guy
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Grioni, Sara
    Groop, Leif C.
    Kaaks, Rudolf
    Key, Timothy J.
    Nilsson, Peter M.
    Overvad, Kim
    Palli, Domenico
    Panico, Salvatore
    Quiros, J. Ramon
    Rolandsson, Olov
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Sacerdote, Carlotta
    Sanchez, Maria-Jose
    Slimani, Nadia
    Teucher, Birgit
    Tjonneland, Anne
    Tumino, Rosario
    van der A, Daphne L.
    Feskens, Edith J. M.
    Langenberg, Claudia
    Forouhi, Nita G.
    Riboli, Elio
    Wareham, Nicholas J.
    Age at Menopause, Reproductive Life Span, and Type 2 Diabetes Risk2013In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 36, no 4, p. 1012-1019Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE-Age at menopause is an important determinant of future health outcomes, but little is known about its relationship with type 2 diabetes. We examined the associations of menopausal age and reproductive life span (menopausal age minus menarcheal age) with diabetes risk.

    RESEARCH DESIGN AND METHODS-Data were obtained from the InterAct study, a prospective case-cohort study nested within the European Prospective Investigation into Cancer and Nutrition. A total of 3,691 postmenopausal type 2 diabetic case subjects and 4,408 subcohort members were included in the analysis, with a median follow-up of 11 years. Prentice weighted Cox proportional hazards models were adjusted for age, known risk factors for diabetes, and reproductive factors, and effect modification by BMI, waist circumference, and smoking was studied.

    RESULTS-Mean (SD) age of the subcohort was 59.2 (5.8) years. After multivariable adjustment, hazard ratios (HRs) of type 2 diabetes were 1.32 (95% CI 1.04-1.69), 1.09 (0.90-1.31), 0.97 (0.86-1.10), and 0.85 (0.70-1.03) for women with menopause at ages <40, 40-44, 45-49, and >= 55 years, respectively, relative to those with menopause at age 50-54 years. The HR per SD younger age at menopause was 1.08 (1.02-1.14). Similarly, a shorter reproductive life span was associated with a higher diabetes risk (HR per SD lower reproductive life span 1.06 [ 1.01-1.12]). No effect modification by BMI, waist circumference, or smoking was observed (P interaction all > 0.05).

    CONCLUSIONS-Early menopause is associated with a greater risk of type 2 diabetes. Diabetes Care 36:1012-1019, 2013

  • 3.
    Dahlquist, G G
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Primary and secondary prevention strategies of pre-type 1 diabetes. Potentials and pitfalls.1999In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 22 Suppl 2, p. B4-6Article in journal (Refereed)
    Abstract [en]

    Over the past decade, a large part of type 1 diabetes research has focused on the possibility of preventing the disease. The objective of this article is to analyze which potential and pitfalls different preventive strategies may involve from the individual, epidemiological, and ethical perspectives. Two potential prevention strategies are considered: l) to try to arrest or delay an already ongoing immune destruction of the beta-cells, and 2) to try to intervene with exposures that may initiate this process. In addition to the potential effects of immune modulation, this prevention strategy depends on screening for risk markers. There are inherent ethical problems with screening because of the introduction of awareness of risk in healthy individuals and also because false positivity, the rate of which differs tremendously in high- and low-risk groups. Because of these latter circumstances, the most promising low-risk preventive treatments presently used in trials, i.e., nicotinamide and insulin, will probably only be feasible in high-risk groups, such as family members, though this group covers only 10-15% of potential cases. The second strategy aiming at eradicating environmental initiators of the beta-cell destruction will avoid the problem of screening and approach a total population at risk. Potential risk factors, such as food components (cow's milk proteins, gliadin or nitroso products) or different viruses, are indicated by animal and epidemiological studies. So far, however, no single environmental risk factor has been proven to be necessary and certainly not sufficient for the disease causation, and the etiological fractions estimated in population-based studies are low. It is concluded that more basic research is warranted before effective and safe prevention can be introduced for type 1 diabetes. Most probably, different preventive strategies must be applied to different groups and populations and in different phases of the beta-cell destruction.

  • 4.
    Dahlquist, G G
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Boman, J E
    Juto, P
    Enteroviral RNA and IgM antibodies in early pregnancy and risk for childhood-onset IDDM in offspring.1999In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 22, no 2, p. 364-5Article in journal (Refereed)
  • 5.
    Dahlquist, G G
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Patterson, C
    Soltesz, G
    Perinatal risk factors for childhood type 1 diabetes in Europe. The EURODIAB Substudy 2 Study Group.1999In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 22, no 10, p. 1698-702Article in journal (Refereed)
    Abstract [en]

    Different perinatal events are associated with an increased risk of type 1 diabetes. The effect of maternal-child blood group incompatibility is strong and indicates a true effect that must be further explored.

  • 6.
    Dahlquist, Gisela G
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Forsberg, Jenny
    Hagenfeldt, Lars
    Boman, Jens
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology.
    Juto, Per
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology.
    Increased prevalence of enteroviral RNA in blood spots from newborn children who later developed type 1 diabetes: a population-based case-control study.2004In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 27, no 1, p. 285-6Article in journal (Refereed)
  • 7.
    Dahlquist, Gisela
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Kallen, Bengt
    Indications that phototherapy is a risk factor for insulin-dependent diabetes.2003In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 26, no 1, p. 247-8Article in journal (Refereed)
  • 8.
    Dahlquist, Gisela
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Nyström, Lennarth
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health.
    Patterson, Christopher C.
    Centre for Public Health, Queen’s University, Belfast, Northern Ireland .
    Incidence of Type 1 Diabetes in Sweden Among Individuals Aged 0-34 Years, 1983-2007: An analysis of time trends2011In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 34, no 8, p. 1754-1759Article in journal (Refereed)
    Abstract [en]

    Objective: To clarify whether the increase in childhood type 1 diabetes is mirrored by a decrease in older age-groups, resulting in younger age at diagnosis.

    Research design and methods: We used data from two prospective research registers, the Swedish Childhood Diabetes Register, which included case subjects aged 0–14.9 years at diagnosis, and the Diabetes in Sweden Study, which included case subjects aged 15–34.9 years at diagnosis, covering birth cohorts between 1948 and 2007. The total database included 20,249 individuals with diabetes diagnosed between 1983 and 2007. Incidence rates over time were analyzed using Poisson regression models.

    Results: The overall yearly incidence rose to a peak of 42.3 per 100,000 person-years in male subjects aged 10–14 years and to a peak of 37.1 per 100,000 person-years in female subjects aged 5–9 years and decreased thereafter. There was a significant increase by calendar year in both sexes in the three age-groups <15 years; however, there were significant decreases in the older age-groups (25- to 29-years and 30- to 34-years age-groups). Poisson regression analyses showed that a cohort effect seemed to dominate over a time-period effect.

    Conclusions: Twenty-five years of prospective nationwide incidence registration demonstrates a clear shift to younger age at onset rather than a uniform increase in incidence rates across all age-groups. The dominance of cohort effects over period effects suggests that exposures affecting young children may be responsible for the increasing incidence in the younger age-groups.

     

  • 9.
    Ekelund, Ulf
    et al.
    Medical Research Council Epidemiology Unit, Cambridge, U.K..
    Franks, Paul
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Sharp, Stephen
    Medical Research Council Epidemiology Unit, Cambridge, U.K..
    Brage, Søren
    Medical Research Council Epidemiology Unit, Cambridge, U.K..
    Wareham, Nicholas J.
    Medical Research Council Epidemiology Unit, Cambridge, U.K..
    Increase in physical activity energy expenditure is associated with reduced metabolic risk independent of change in fatness and fitness2007In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 30, no 8, p. 2101-2106Article in journal (Refereed)
    Abstract [en]

    Objective: We sought to examine whether change in physical activity energy expenditure (PAEE) is associated with change in metabolic risk factors and whether this association is independent of change in fat mass and aerobic fitness.

    Research design and methods: In a population-based sample of 176 men and 217 women followed prospectively for 5.6 years, we measured PAEE by individually calibrated heart rate monitoring, aerobic fitness, total body fat (fat mass), and metabolic risk factors (blood pressure, fasting triglycerides, HDL cholesterol, insulin, and 2-h glucose) at baseline and follow-up.

    Results: A 100 J · kg fat-free mass (FFM)−1 · min−1 increase in PAEE from baseline to follow-up reduced triglycerides by 3.5% (95% CI 0.03–5.7) in men and 3.2% (0.02–5.4) in women, fasting insulin by 5.3% (1.0–7.5) in men and women, and 2-h glucose by 3.2% (0.3–5.3) in men and 3.1% (0.3–5.2) in women, after adjustment for sex, age, smoking status, aerobic fitness, baseline phenotype, and change in fat mass. In general, the magnitudes of association for change in fat mass with metabolic risk factors were two to three times stronger than for PAEE.

    Conclusions: Increasing levels of physical activity may protect against metabolic disease even in the absence of improved aerobic fitness and reduced body fatness. Therefore, the combination of increasing levels of physical activity and avoidance of gain in fat mass is likely to be the most successful approach for preventing cardiovascular and metabolic disease.

  • 10. Elks, Cathy E.
    et al.
    Ong, Ken K.
    Scott, Robert A.
    van der Schouw, Yvonne T.
    Brand, Judith S.
    Wark, Petra A.
    Amiano, Pilar
    Balkau, Beverley
    Barricarte, Aurelio
    Boeing, Heiner
    Fonseca-Nunes, Ana
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Lunds universitet.
    Grioni, Sara
    Halkjaer, Jytte
    Kaaks, Rudolf
    Key, Timothy J.
    Khaw, Kay Tee
    Mattiello, Amalia
    Nilsson, Peter M.
    Overvad, Kim
    Palli, Domenico
    Quiros, J. Ramon
    Rinaldi, Sabina
    Rolandsson, Olov
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Romieu, Isabelle
    Sacerdote, Carlotta
    Sanchez, Maria-Jose
    Spijkerman, Annemieke M. W.
    Tjonneland, Anne
    Tormo, Maria-Jose
    Tumino, Rosario
    Daphne, L. Van der A.
    Forouhi, Nita G.
    Sharp, Stephen J.
    Langenberg, Claudia
    Riboli, Elio
    Wareham, Nicholas J.
    Age at Menarche and Type 2 Diabetes Risk The EPIC-InterAct study2013In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 36, no 11, p. 3526-3534Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE Younger age at menarche, a marker of pubertal timing in girls, is associated with higher risk of later type 2 diabetes. We aimed to confirm this association and to examine whether it is explained by adiposity. RESEARCH DESIGN AND METHODS The prospective European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct case-cohort study consists of 12,403 incident type 2 diabetes cases and a stratified subcohort of 16,154 individuals from 26 research centers across eight European countries. We tested the association between age at menarche and incident type 2 diabetes using Prentice-weighted Cox regression in 15,168 women (n = 5,995 cases). Models were adjusted in a sequential manner for potential confounding and mediating factors, including adult BMI. RESULTS Mean menarcheal age ranged from 12.6 to 13.6 years across InterAct countries. Each year later menarche was associated with 0.32 kg/m(2) lower adult BMI. Women in the earliest menarche quintile (8-11 years, n = 2,418) had 70% higher incidence of type 2 diabetes compared with those in the middle quintile (13 years, n = 3,634), adjusting for age at recruitment, research center, and a range of lifestyle and reproductive factors (hazard ratio [HR], 1.70; 95% CI, 1.49-1.94; P < 0.001). Adjustment for BMI partially attenuated this association (HR, 1.42; 95% CI, 1.18-1.71; P < 0.001). Later menarche beyond the median age was not protective against type 2 diabetes. CONCLUSIONS Women with history of early menarche have higher risk of type 2 diabetes in adulthood. Less than half of this association appears to be mediated by higher adult BMI, suggesting that early pubertal development also may directly increase type 2 diabetes risk.

  • 11.
    Estampador, Angela C.
    et al.
    Genetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Skåne University Hospital, Lund University, Malmö, Sweden .
    Pomeroy, Jeremy
    Genetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Skåne University Hospital, Lund University, Malmö, Sweden ; Phoenix Epidemiology and Clinical Research Branch, National Institutes of Health, Phoenix, AZ .
    Renström, Frida
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Genetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Skåne University Hospital, Lund University, Malmö, Sweden .
    Nelson, Scott M.
    Reproductive and Maternal Medicine, Faculty of Medicine, University of Glasgow, Glasgow, U.K..
    Mogren, Ingrid
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynaecology.
    Persson, Margareta
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynaecology. Dalarna University, School of Health and Social Studies, Falun, Sweden.
    Sattar, Naveed
    British Heart Foundation Cardiovascular Research Center, University of Glasgow, Glasgow, U.K..
    Domellöf, Magnus
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Genetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Skåne University Hospital, Lund University, Malmö, Sweden ; Department of Nutrition, Harvard School of Public Health, Boston, MA.
    Infant body composition and adipokine concentrations in relation to maternal gestational weight gain2014In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 37, no 5, p. 1432-1438Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To investigate associations of maternal gestational weight gain and body composition and their impact on offspring body composition and adipocytokine, glucose, and insulin concentrations at age 4 months. RESEARCH DESIGN AND METHODS: This was a prospective study including 31 mother-infant pairs (N = 62). Maternal body composition was assessed using doubly labeled water. Infant body composition was assessed at 4 months using air displacement plethysmography, and venous blood was assayed for glucose, insulin, adiponectin, interleukin-6 (IL-6), and leptin concentrations. RESULTS: Rate of gestational weight gain in midpregnancy was significantly associated with infant fat mass (r = 0.41, P = 0.03); rate of gestational weight in late pregnancy was significantly associated with infant fat-free mass (r = 0.37, P = 0.04). Infant birth weight was also strongly correlated with infant fat-free mass at 4 months (r = 0.63, P = 0.0002). Maternal BMI and maternal fat mass were strongly inversely associated with infant IL-6 concentrations (r = -0.60, P = 0.002 and r = -0.52, P = 0.01, respectively). Infant fat-free mass was inversely related to infant adiponectin concentrations (r = -0.48, P = 0.008) and positively correlated with infant blood glucose adjusted for insulin concentrations (r = 0.42, P = 0.04). No significant associations for leptin were observed. CONCLUSIONS: Timing of maternal weight gain differentially impacts body composition of the 4-month-old infant, which in turn appears to affect the infant's glucose and adipokine concentrations.

  • 12.
    Franks, Paul W.
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Pearson, Ewan
    Florez, Jose C.
    Gene-Environment and Gene-Treatment Interactions in Type 2 Diabetes2013In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 36, no 5, p. 1413-1421Article, review/survey (Refereed)
  • 13. Goedecke, Julia H
    et al.
    Dave, Joel A
    Faulenbach, Mirjam V
    Utzschneider, Kristina M
    Lambert, Estelle V
    West, Sacha
    Collins, Malcolm
    Olsson, Tommy
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Walker, Brian R
    Seckl, Jonathan R
    Kahn, Steven E
    Levitt, Naomi S
    Insulin response in relation to insulin sensitivity: an appropriate beta-cell response in black South African women.2009In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 32, no 5, p. 860-855Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: The purpose of this study was to characterize differences in the acute insulin response to glucose (AIR(g)) relative to insulin sensitivity (S(I)) in black and white premenopausal normoglycemic South African women matched for body fatness. RESEARCH DESIGN AND METHODS: Cross-sectional analysis including 57 black and white South African women matched for BMI, S(I), AIR(g), and the disposition index (AIR(g) x S(I)) were performed using a frequently sampled intravenous glucose tolerance test with minimal model analysis, and similar measures were analyzed using an oral glucose tolerance test (OGTT). Body composition was assessed by dual-energy X-ray absorptiometry and computed tomography. RESULTS: S(I) was significantly lower (4.4 +/- 0.8 vs. 9.4 +/- 0.8 and 2.9 +/- 0.8 vs. 6.0 +/- 0. 8 x 10(-5) min(-1)/[pmol/l], P < 0.001) and AIR(g) was significantly higher (1,028 +/- 255 vs. 352 +/- 246 and 1,968 +/- 229 vs. 469 +/- 246 pmol/l, P < 0.001), despite similar body fatness (30.9 +/- 1.4 vs. 29.7 +/- 1.3 and 46.8 +/- 1.2 vs. 44.4 +/- 1.3%) in the normal-weight and obese black women compared with their white counterparts, respectively. Disposition index, a marker of beta-cell function, was not different between ethnic groups (3,811 +/- 538 vs. 2,966 +/- 518 and 3,646 +/- 485 vs. 2,353 +/- 518 x 10(-5) min, P = 0.10). Similar results were obtained for the OGTT-derived measures. CONCLUSIONS: Black South African women are more insulin resistant than their white counterparts but compensate by increasing their insulin response to maintain normal glucose levels, suggesting an appropriate beta-cell response for the level of insulin sensitivity.

  • 14. Hare, Matthew JL
    et al.
    Magliano, Dianna J
    Zimmet, Paul Z
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Joonas, Noorjehan
    Pauvaday, Vassen
    Larhubarbe, Jose
    Tuomilehto, Jaakko
    Kowlessur, Sudhir
    Alberti, K George MM
    Shaw, Jonathan E
    Glucose-independent ethnic differences in HbA(1c), in people without known diabetes2013In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 36, no 6, p. 1534-1540Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE To determine whether glucose-independent differences in HbA(1c) exist between people of African, South Asian, and Chinese ethnicities.

    RESEARCH DESIGN AND METHODS Data from 6,701 people aged 19-78 years, without known diabetes, from Mauritius, and participating in the population-based Non-Communicable Disease Surveys of the main island and the island of Rodrigues were included. Participants were African (n = 1,219 from main island, n = 1,505 from Rodrigues), South Asian (n = 3,820), and Chinese (n = 157). Survey data included HbA(1c), plasma glucose during oral glucose tolerance testing (OGTT), anthropometry, demographics, and medical and lifestyle history.

    RESULTS Mean HbA(1c), after adjustment for fasting and 2-h plasma glucose and other factors known to influence HbA(1c), was higher in Africans from Rodrigues (6.1%) than in South Asians (5.7%, P < 0.001), Chinese (5.7%, P < 0.001), or Africans from the main island of Mauritius (5.7%, P < 0.001). The age-standardized prevalence of diabetes among Africans from Rodrigues differed substantially depending on the diagnostic criteria used [OGTT 7.9% (95% CI 5.8-10.0); HbA(1c) 17.3% (15.3-19.2)]. Changing diagnostic criteria resulted in no significant change in the prevalence of diabetes within the other ethnic groups.

    CONCLUSIONS People of African ethnicity from Rodrigues have higher HbA(1c) than those of South Asian or African ethnicity from the main island of Mauritius for reasons not explained by plasma glucose during an OGTT or traditional factors known to affect glycemia. Further research should be directed at determining the mechanism behind this disparity and its relevance to clinical outcomes.

  • 15. Hyvärinen, Marjukka
    et al.
    Qiao, Qing
    Tuomilehto, Jaakko
    Laatikainen, Tiina
    Heine, Robert J
    Stehouwer, Coen D A
    Alberti, K George M M
    Pyörälä, Kalevi
    Zethelius, Björn
    Stegmayr, Birgitta
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine.
    Hyperglycemia and stroke mortality: comparison between fasting and 2-h glucose criteria.2009In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 32, no 2, p. 348-354Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: We investigated stroke mortality in individuals in different categories of glycemia and compared hazard ratios (HRs) corresponding to a 1-SD increase in 2-h plasma glucose and fasting plasma glucose (FPG) criteria. RESEARCH DESIGN AND METHODS: We examined data from 2-h 75-g oral glucose tolerance tests taken from 13 European cohorts comprising 11,844 (55%) men and 9,862 (45%) women who were followed up for a median of 10.5 years. A multivariate adjusted Cox proportional hazards model was used to estimate HRs for stroke mortality. RESULTS: In men and women without a prior history of diabetes, multivariate adjusted HRs for stroke mortality corresponding to a 1-SD increase in FPG were 1.02 (95% CI 0.83-1.25) and 1.52 (1.22-1.88) and those in 2-h plasma glucose 1.21 (1.06-1.38) and 1.31 (1.06-1.61), respectively. Addition of 2-h plasma glucose to the model with FPG significantly improved prediction of stroke mortality in men (chi2 = 10.12; P = 0.001) but not in women (chi2 = 0.01; P = 0.94), whereas addition of FPG to 2-h plasma glucose improved stroke mortality in women (chi2 = 4.08; P = 0.04) but not in men (chi2 = 3.29; P = 0.07). CONCLUSIONS: Diabetes defined by either FPG or 2-h plasma glucose increases the risk of stroke mortality. In individuals without a history of diabetes, elevated 2-h postchallenge glucose is a better predictor than elevated fasting glucose in men, whereas the latter is better than the former in women.

  • 16.
    Krachler, Benno
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Comment on Juraschek et al. Cardiorespiratory Fitness and Incident Diabetes: The FIT (Henry Ford ExercIse Testing) Project. Diabetes Care 2015;38:1075-10812015In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 38, no 11, p. e193-Article in journal (Other academic)
  • 17.
    Magliano, Dianna J
    et al.
    Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Zimmet, Paul Z
    Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
    Cartensen, Bendix
    Steno Diabetes Center, Gentofte, Denmark, and Department of Biostatistics, University of Copenhagen, Copenhagen, Denmark.
    Balkau, Beverly
    Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
    Pauvaday, Vassen
    Ministry of Health and Quality of Life, Island of Mauritius.
    Kowlessur, Sudhir
    Ministry of Health and Quality of Life, Island of Mauritius.
    Tuomilehto, Jaakko
    Hjelt Institute, Department of Public Health, University of Helsinki, Helsinki, Finland.
    Alberti, K George M M
    Department of Endocrinology and Metabolism, St. Mary's Hospital and Imperial College, London, U.K..
    Shaw, Jonathan E
    Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
    Mortality, all-cause and cardiovascular disease, over 15 years in multiethnic mauritius: impact of diabetes and intermediate forms of glucose tolerance2010In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 33, no 9, p. 1983-1989Article in journal (Refereed)
    Abstract [en]

    This is the first study in a developing country of the impact of glucose intolerance on mortality in an African population, and one of the first studies of a South Asian population. It shows that the impact on mortality in these populations in Mauritius is comparable to that seen in developed countries. These results are important in a global context for future health policy in light of the impact of the rapid increase in prevalence of diabetes, especially in developing nations.

  • 18. Magliano, Dianna J
    et al.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Zimmet, Paul Z
    Chen, Lei
    Joonas, Noorjehan
    Kowlessur, Sudhir
    Larhubarbe, Jose
    Gaoneadry, Dhanunjaye
    Pauvaday, Vassen
    Tuomilehto, Jaakko
    Alberti, K George MM
    Shaw, Jonathan E
    Explaining the increase of diabetes prevalence and plasma glucose in Mauritius2012In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 35, no 1, p. 87-91Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE Secular trends in the epidemiology of diabetes are best described by studying the same population over time, but few such studies exist. Using surveys from Mauritius in 1987 and 2009, we examined 1) the change in the prevalence of diabetes, 2) the extent to which changes in traditional diabetes risk factors explained the increase, and 3) the change in the distribution of plasma glucose levels over time.

    RESEARCH DESIGN AND METHODS Independent population-based surveys were undertaken in Mauritius in 1987 and 2009 using similar methodology in adults aged 20-74 years. Physical measurements and fasting blood samples were taken, and an oral glucose tolerance test was performed at both surveys.

    RESULTS The age-standardized prevalence of diabetes in 2009 was 22.3% (95% CI 20.0-24.6) among men and 20.2% (18.3-22.3) among women, representing an increase since 1987 of 64 and 62% among men and women, respectively. Concurrent changes in the distribution of age, ethnicity, waist circumference, BMI, physical activity, smoking, family history of diabetes, and hypertension explained more of the increase in the prevalence of diabetes in men than in women. Increases in plasma glucose (especially fasting glucose) were seen across the population but were greater at the upper levels.

    CONCLUSIONS In Mauritius, there has been a marked increase in diabetes prevalence over 22 years. This mainly results from changes in traditional risk factors, leading to population-wide increases in plasma glucose levels. Interventions to control this escalation of diabetes should focus on population-wide strategies.

  • 19. Meidtner, Karina
    et al.
    Podmore, Clara
    Kroger, Janine
    van der Schouw, Yvonne T.
    Bendinelli, Benedetta
    Agnoli, Claudia
    Arriola, Larraitz
    Barricarte, Aurelio
    Boeing, Heiner
    Cross, Amanda J.
    Dow, Courtney
    Ekblom, Kim
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Fagherazzi, Guy
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine. Department of Clinical Sciences, Lund University, Malmö, Sweden.
    Gunter, Marc J.
    Huerta, Jose Maria
    Jakszyn, Paula
    Jenab, Mazda
    Katzke, Verena A.
    Key, Timothy J.
    Khaw, Kay Tee
    Kuhn, Tilman
    Kyro, Cecilie
    Mancini, Francesca Romana
    Melander, Olle
    Nilsson, Peter M.
    Overvad, Kim
    Palli, Domenico
    Panico, Salvatore
    Quiros, J. Ramon
    Rodriguez-Barranco, Miguel
    Sacerdote, Carlotta
    Sluijs, Ivonne
    Stepien, Magdalena
    Tjonneland, Anne
    Tumino, Rosario
    Forouhi, Nita G.
    Sharp, Stephen J.
    Langenberg, Claudia
    Schulze, Matthias B.
    Riboli, Elio
    Wareham, Nicholas J.
    Interaction of Dietary and Genetic Factors Influencing Body Iron Status and Risk of Type 2 Diabetes Within the EPIC-InterAct Study2018In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 41, no 2, p. 277-285Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Meat intake has been consistently shown to be positively associated with incident type 2 diabetes. Part of that association may be mediated by body iron status, which is influenced by genetic factors. We aimed to test for interactions of genetic and dietary factors influencing body iron status in relation to the risk of incident type 2 diabetes.

    RESEARCH DESIGN AND METHODS: The case-cohort comprised 9,347 case subjects and 12,301 subcohort participants from eight European countries. Single nucleotide polymorphisms (SNPs) were selected from genome-wide association studies on iron status biomarkers and candidate gene studies. A ferritin-related gene score was constructed. Multiplicative and additive interactions of heme iron and SNPs as well as the gene score were evaluated using Cox proportional hazards regression.

    RESULTS: Higher heme iron intake (per 1 SD) was associated with higher ferritin levels (β = 0.113 [95% CI 0.082; 0.144]), but not with transferrin (−0.019 [−0.043; 0.006]) or transferrin saturation (0.016 [−0.006; 0.037]). Five SNPs located in four genes (rs1799945 [HFE H63D], rs1800562 [HFE C282Y], rs236918 [PCK7], rs744653 [SLC40A1], and rs855791 [TMPRSS6V736A]) were associated with ferritin. We did not detect an interaction of heme iron and the gene score on the risk of diabetes in the overall study population (Padd = 0.16, Pmult = 0.21) but did detect a trend toward a negative interaction in men (Padd = 0.04, Pmult = 0.03).

    CONCLUSIONS: We found no convincing evidence that the interplay of dietary and genetic factors related to body iron status associates with type 2 diabetes risk above the level expected from the sum or product of the two individual exposures.

  • 20.
    Möllsten, Anna
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Dahlquist, Gisela
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Stattin, Eva-Lena
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Medical and Clinical Genetics.
    Rudberg, Susanne
    Higher intakes of fish protein are related to a lower risk of microalbuminuria in young Swedish type 1 diabetic patients.2001In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 24, no 5, p. 805-810Article in journal (Refereed)
  • 21. Nettleton, Jennifer A
    et al.
    McKeown, Nicola M
    Kanoni, Stavroula
    Lemaitre, Rozenn N
    Hivert, Marie-France
    Ngwa, Julius
    van Rooij, Frank J A
    Sonestedt, Emily
    Wojczynski, Mary K
    Ye, Zheng
    Tanaka, Toshiko
    Garcia, Melissa
    Anderson, Jennifer S
    Follis, Jack L
    Djousse, Luc
    Mukamal, Kenneth
    Papoutsakis, Constantina
    Mozaffarian, Dariush
    Zillikens, M Carola
    Bandinelli, Stefania
    Bennett, Amanda J
    Borecki, Ingrid B
    Feitosa, Mary F
    Ferrucci, Luigi
    Forouhi, Nita G
    Groves, Christopher J
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Harris, Tamara
    Hofman, Albert
    Houston, Denise K
    Hu, Frank B
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Kritchevsky, Stephen B
    Langenberg, Claudia
    Launer, Lenore
    Liu, Yongmei
    Loos, Ruth J
    Nalls, Michael
    Orho-Melander, Marju
    Renström, Frida
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Rice, Kenneth
    Riserus, Ulf
    Rolandsson, Olov
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Rotter, Jerome I
    Saylor, Georgia
    Sijbrands, Eric JG
    Sjögren, Per
    Smith, Albert
    Steingrímsdóttir, Laufey
    Uitterlinden, André G
    Wareham, Nicholas J
    Prokopenko, Inga
    Pankow, James S
    van Duijn, Cornelia M
    Flores, Jose C
    Witteman, Jaqueline CM
    Dupuis, Josée
    Dedoussis, George V
    Ordovas, Jose M
    Ingelsson, Erik
    Cupples, L Adrienne
    Siscovick, David S
    Franks, Paul W
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Meigs, James B
    Interactions of dietary whole-grain intake with fasting glucose- and insulin-related genetic loci in individuals of European descent: a meta-analysis of 14 cohort studies2010In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 33, no 12, p. 2684-2691Article in journal (Refereed)
    Abstract [en]

    Our results support the favorable association of whole-grain intake with fasting glucose and insulin and suggest a potential interaction between variation in GCKR and whole-grain intake in influencing fasting insulin concentrations.

  • 22.
    Ning, Feng
    et al.
    Department of Public Health, University of Helsinki, Helsinki, Finland.
    Tuomilehto, Jaakko
    Department of Public Health, University of Helsinki, Helsinki, Finland.
    Pyörälä, Kalevi
    Institute of Clinical Medicine, Faculty of Health Sciences, University of Eastern Finland, Kuopio, Finland.
    Onat, Altan
    Turkish Society of Cardiology, Istanbul, Turkey.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Qiao, Qing
    Department of Public Health, University of Helsinki, Helsinki, Finland.
    Cardiovascular disease mortality in Europeans in relation to fasting and 2-h plasma glucose levels within a normoglycemic range2010In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 33, no 10, p. 2211-2216Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE To study mortality in relation to fasting plasma glucose (FPG) and 2-h plasma glucose levels within the normoglycemic range.

    RESEARCH DESIGN AND METHODS Data from 19 European cohorts comprising 12,566 men and 10,874 women who had FPG <6.1 mmol/l and 2-h plasma glucose <7.8 mmol/l at baseline examination were analyzed. Multivariate-adjusted hazard ratios (HRs) and 95% CIs for deaths from cardiovascular disease (CVD), non-CVD, and all causes were estimated for individuals whose 2-h plasma glucose > FPG (group II) compared with those whose 2-h plasma glucose ≤ FPG (group I).

    RESULTS A total of 827 (246) CVD and 611 (351) non-CVD and 1,438 (597) all-cause deaths occurred in men (women). Group II was older and had higher BMI, blood pressure, and fasting insulin than group I. The multivariate-adjusted HRs (95% CIs) for CVD, non-CVD, and all-cause mortality were 1.22 (1.05–1.41), 1.09 (0.92–1.29), and 1.16 (1.04–1.30) in men and 1.40 (1.03–1.89), 0.99 (0.79–1.25), and 1.13 (0.94–1.35) in women, respectively, for group II as compared with group I. HRs were 1.25 (1.05–1.50), 1.09 (0.89–1.34), and 1.18 (1.03–1.35) in men and 1.60 (1.03–2.48), 1.05 (0.78–1.42), and 1.18 (0.93–1.51) in women, respectively, after additional adjustment for fasting insulin in a subgroup of individuals.

    CONCLUSIONS In individuals with both FPG and 2-h plasma glucose within the normoglycemic range, high 2-h plasma glucose was associated with insulin resistance and increased CVD mortality.

  • 23. Nyberg, Solja T.
    et al.
    Fransson, Eleonor I.
    Heikkila, Katriina
    Ahola, Kirsi
    Alfredsson, Lars
    Bjorner, Jakob B.
    Borritz, Marianne
    Burr, Hermann
    Dragano, Nico
    Goldberg, Marcel
    Hamer, Mark
    Jokela, Markus
    Knutsson, Anders
    Koskenvuo, Markku
    Koskinen, Aki
    Kouvonen, Anne
    Leineweber, Constanze
    Madsen, Ida E. H.
    Hanson, Linda L. Magnusson
    Marmot, Michael G.
    Nielsen, Martin L.
    Nordin, Maria
    Umeå University, Faculty of Social Sciences, Department of Psychology.
    Oksanen, Tuula
    Pejtersen, Jan H.
    Pentti, Jaana
    Rugulies, Reiner
    Salo, Paula
    Siegrist, Johannes
    Steptoe, Andrew
    Suominen, Sakari
    Theorell, Tores
    Vaananen, Ari
    Vahtera, Jussi
    Virtanen, Marianna
    Westerholm, Peter J. M.
    Westerlund, Hugo
    Zins, Marie
    Batty, G. David
    Brunner, Eric J.
    Ferrie, Jane E.
    Singh-Manoux, Archana
    Kivimaki, Mika
    Job Strain as a Risk Factor for Type 2 Diabetes: A Pooled Analysis of 124,808 Men and Women2014In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 37, no 8, p. 2268-2275Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE The status of psychosocial stress at work as a risk factor for type 2 diabetes is unclear because existing evidence is based on small studies and is subject to confounding by lifestyle factors, such as obesity and physical inactivity. This collaborative study examined whether stress at work, defined as "job strain," is associated with incident type 2 diabetes independent of lifestyle factors. RESEARCH DESIGN AND METHODS We extracted individual-level data for 124,808 diabetes-free adults from 13 European cohort studies participating in the IPD-Work Consortium. We measured job strain with baseline questionnaires. Incident type 2 diabetes at follow-up was ascertained using national health registers, clinical screening, and self-reports. We analyzed data for each study using Cox regression and pooled the study-specific estimates in fixed-effect meta-analyses. RESULTS There were 3,703 cases of incident diabetes during a mean follow-up of 10.3 years. After adjustment for age, sex, and socioeconomic status (SES), the hazard ratio (HR) for job strain compared with no job strain was 1.15 (95% CI 1.06-1.25) with no difference between men and women (1.19 [1.06-1.34] and 1.13 [1.00-1.28], respectively). In stratified analyses, job strain was associated with an increased risk of diabetes among those with healthy and unhealthy lifestyle habits. In a multivariable model adjusted for age, sex, SES, and lifestyle habits, the HR was 1.11 (1.00-1.23). CONCLUSIONS Findings from a large pan-European dataset suggest that job strain is a risk factor for type 2 diabetes in men and women independent of lifestyle factors.

  • 24. Podmore, Clara
    et al.
    Meidtner, Karina
    Schulze, Matthias B.
    Scott, Robert A.
    Ramond, Anna
    Butterworth, Adam S.
    Di Angelantonio, Emanuele
    Danesh, John
    Arriola, Larraitz
    Barricarte, Aurelio
    Boeing, Heiner
    Clavel-Chapelon, Francoise
    Cross, Amanda J.
    Dahm, Christina C.
    Fagherazzi, Guy
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Gavrila, Diana
    Grioni, Sara
    Gunter, Marc J.
    Gusto, Gaelle
    Jakszyn, Paula
    Katzke, Verena
    Key, Timothy J.
    Kuhn, Tilman
    Mattiello, Amalia
    Nilsson, Peter M.
    Olsen, Anja
    Overvad, Kim
    Palli, Domenico
    Ramon Quiros, J.
    Rolandsson, Olov
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Sacerdote, Carlotta
    Sanchez-Cantalejo, Emilio
    Slimani, Nadia
    Sluijs, Ivonne
    Spijkerman, Annemieke M. W.
    Tjonneland, Anne
    Tumino, Rosario
    van der A, Daphne L.
    van der Schouw, Yvonne T.
    Feskens, Edith J. M.
    Forouhi, Nita G.
    Sharp, Stephen J.
    Riboli, Elio
    Langenberg, Claudia
    Wareham, Nicholas J.
    Association of Multiple Biomarkers of Iron Metabolism and Type 2 Diabetes: The EPIC-InterAct Study2016In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 39, no 4, p. 572-581Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE Observational studies show an association between ferritin and type 2 diabetes (T2D), suggesting a role of high iron stores in T2D development. However, ferritin is influenced by factors other than iron stores, which is less the case for other biomarkers of iron metabolism. We investigated associations of ferritin, transferrin saturation (TSAT), serum iron, and transferrin with T2D incidence to clarify the role of iron in the pathogenesis of T2D.

    RESEARCH DESIGN AND METHODS The European Prospective Investigation into Cancer and Nutrition-InterAct study includes 12,403 incident T2D cases and a representative subcohort of 16,154 individuals from a European cohort with 3.99 million person-years of follow-up. We studied the prospective association of ferritin, TSAT, serum iron, and transferrin with incident T2D in 11,052 cases and a random subcohort of 15,182 individuals and assessed whether these associations differed by subgroups of the population.

    RESULTS Higher levels of ferritin and transferrin were associated with a higher risk of T2D (hazard ratio [HR] [95% CI] in men and women, respectively: 1.07 [1.01-1.12] and 1.12 [1.05-1.19] per 100mg/L higher ferritin level; 1.11 [1.00-1.24] and 1.22 [1.12-1.33] per 0.5 g/L higher transferrin level) after adjustment for age, center, BMI, physical activity, smoking status, education, hs-CRP, alanine aminotransferase, and g-glutamyl transferase. Elevated TSAT (>= 45% vs. <45%) was associated with a lower risk of T2D in women (0.68 [0.54-0.86]) but was not statistically significantly associated in men (0.90 [0.75-1.08]). Serum iron was not associated with T2D. The association of ferritin with T2D was stronger among leaner individuals (P-interaction < 0.01).

    CONCLUSIONS The pattern of association of TSAT and transferrin with T2D suggests that the underlying relationship between iron stores and T2D is more complex than the simple link suggested by the association of ferritin with T2D.

  • 25. Pomeroy, Jeremy
    et al.
    Renström, Frida
    Gradmark, Anna
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Mogren, Ingrid
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynaecology.
    Persson, Margareta
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynaecology.
    Bluck, Les
    Wright, Antony
    Kahn, Steven E.
    Domellöf, Magnus
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Maternal Physical Activity and Insulin Action in Pregnancy and Their Relationships With Infant Body Composition2013In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 36, no 2, p. 267-269Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE-We sought to assess the association between maternal gestational physical activity and insulin action and body composition in early infancy. RESEARCH DESIGN AND METHODS-At 28-32 weeks' gestation, pregnant women participating in an observational study in Sweden underwent assessments of height, weight, and body composition, an oral glucose tolerance test, and 10 days of objective physical activity assessment. Thirty mothers and infants returned at 11-19 weeks postpartum. Infants underwent assessments of weight, length, and body composition. RESULTS-Early insulin response was correlated with total physical activity (r = 0.47; P = 0.007). Early insulin response (r = -0.36; P = 0.045) and total physical activity (r = 0.52; P = 0.037) were also correlated with infant fat-free mass. No maternal variable was significantly correlated with infant adiposity. CONCLUSIONS-The relationships between maternal physical activity, insulin response, and infant fat-free mass suggest that physical activity during pregnancy may affect metabolic outcomes in the mother and her offspring. 

  • 26.
    Pourhamidi, Kaveh
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Dahlin, Lars B
    Department of Clinical Sciences Malmö, Hand Surgery, Skåne University Hospital, Lund University, Malmö, Sweden.
    Englund, Elisabet
    Division of Neuropathology, Department of Pathology, Lund University, Lund, Sweden.
    Rolandsson, Olov
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    No difference in small or large nerve fiber function between individuals with normal glucose tolerance and impaired glucose tolerance2013In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 36, no 4, p. 962-964Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE To assess small and large nerve fiber function in people with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and type 2 diabetes (T2D).

    RESEARCH DESIGN AND METHODS Participants were recruited consecutively from a population-based cohort: NGT (n = 39), IGT (n = 29), and T2D (n = 51). Electrophysiological measures included nerve conduction studies and thermal thresholds. Intraepidermal nerve fiber density (IENFD) in skin biopsies was calculated.

    RESULTS There was no difference between IGT and NGT in sural nerve conduction, IENFD, and thermal thresholds. IENFD was significantly lower in T2D (median = 2.8 fibers/mm [Interquartile range 1.1–4.7 fibers/mm]) than NGT individuals (4.5 fibers/mm [3.4–6.1 fibers/mm]; P < 0.05). T2D participants had poorer nerve conduction and higher heat thresholds than NGT and IGT.

    CONCLUSIONS Large and small nerve function in people with IGT did not differ from those with NGT. Our finding does not support the existence of neuropathy in a prediabetic stage.

  • 27.
    Pourhamidi, Kaveh
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Skärstrand, Hanna
    Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Sweden .
    Dahlin, Lars B.
    Department of Clinical Sciences, Malmö, Hand Surgery, Skåne University Hospital, Lund University, Malmö, Sweden .
    Rolandsson, Olov
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    HSP27 concentrations are lower in patients with type 1 diabetes and correlate with large nerve fiber dysfunction2014In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 37, no 3, p. E49-E50Article in journal (Other academic)
  • 28. Rask, Eva
    et al.
    Olsson, Tommy
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Johnson, Owe
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Seckl, J
    Holst, J J
    Ahrén, B
    Impaired incretin response after a mixed meal is associated with insulin resistance in nondiabetic men.2001In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 24, no 9, p. 1640-1645Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To investigate whether features of the insulin resistance syndrome are associated with altered incretin responses to food intake.

    RESEARCH DESIGN AND METHODS: From a population-based study, 35 men were recruited, representing a wide spectrum of insulin sensitivity and body weight. Each subject underwent a hyperinsulinemic-euglycemic clamp to determine insulin sensitivity. A mixed meal was given, and plasma levels of gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1), as well as insulin, glucagon, and glucose were measured.

    RESULTS: Insulin resistance was associated with impaired GIP and GLP-1 responses to a mixed meal. The total area under the curve (AUC) of the GIP response after the mixed meal was associated with insulin sensitivity (r = 0.54, P < 0.01). There was a significant difference between the highest and the lowest tertile of insulin sensitivity (P < 0.05). GLP-1 levels 15 min after food intake were significantly lower in the most insulin-resistant tertile compared with the most insulin-sensitive tertile. During the first hour, the AUC of GLP-1 correlated significantly with insulin sensitivity (r = 0.47, P < 0.01). Multiple linear regression analysis showed that insulin resistance, but not obesity, was an independent predictor of these decreased incretin responses.

    CONCLUSIONS: In insulin resistance, the GIP and GLP-1 responses to a mixed meal are impaired and are related to the degree of insulin resistance. Decreased incretin responsiveness may be of importance for the development of impaired glucose tolerance.

  • 29.
    Rolandsson, Olov
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Hampe, Christiane S
    Wennberg, Patrik
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Radtke, Jared
    Langenberg, Claudia
    Wareham, Nicholas
    Prevalence and Regional Distribution of Autoantibodies Against GAD65Ab in a European Population Without Diabetes: The EPIC-InterAct Study2015In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 38, no 8, p. E114-E115Article in journal (Refereed)
  • 30.
    Rolandsson, Olov
    et al.
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Family Medicine.
    Risborg, O
    Rasmark, S
    Distal symmetric polyneuropathy is uncommon in impaired glucose tolerance.: Conference Information: 67th Annual Meeting of the American-Diabetes-Association2008In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 57, no suppl 1, p. A224-A224Article in journal (Refereed)
  • 31.
    Ruge, Toralph
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery.
    Nyström, Lennarth
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Norberg, Margareta
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Weinehall, Lars
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Rolandsson, Olov
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Recruiting high-risk individuals to a diabetes prevention program: how hard can it be?2007In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 30, no 7, p. e61-Article in journal (Refereed)
  • 32. Spijkerman, Annemieke M. W.
    et al.
    van der A, Daphne L.
    Nilsson, Peter M.
    Ardanaz, Eva
    Gavrila, Diana
    Agudo, Antonio
    Arriola, Larraitz
    Balkau, Beverley
    Beulens, Joline W.
    Boeing, Heiner
    de Lauzon-Guillain, Blandine
    Fagherazzi, Guy
    Feskens, Edith J. M.
    Franks, Paul
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Grioni, Sara
    Huerta, Jose Maria
    Kaaks, Rudolf
    Key, Timothy J.
    Overvad, Kim
    Palli, Domenico
    Panico, Salvatore
    Redondo, M. Luisa
    Rolandsson, Olov
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Roswal, Nina
    Sacerdote, Carlotta
    Sanchez, Maria-Jose
    Schulze, Matthias B.
    Slimani, Nadia
    Teucher, Birgit
    Tjonneland, Anne
    Tumino, Rosario
    van der Schouw, Yvonne T.
    Langenberg, Claudia
    Sharp, Stephen J.
    Forouhi, Nita G.
    Riboli, Elio
    Wareham, Nicholas J.
    Smoking and Long-Term Risk of Type 2 Diabetes: The EPIC-InterAct Study in European Populations2014In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 37, no 12, p. 3164-3171Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE

    The aims of this study were to investigate the association between smoking and incident type 2 diabetes, accounting for a large number of potential confounding factors, and to explore potential effect modifiers and intermediate factors.

    RESEARCH DESIGN AND METHODS

    The European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct is a prospective case-cohort study within eight European countries, including 12,403 cases of incident type 2 diabetes and a random subcohort of 16,835 individuals. After exclusion of individuals with missing data, the analyses included 10,327 cases and 13,863 subcohort individuals. Smoking status was used (never, former, current), with never smokers as the reference. Country-specific Prentice-weighted Cox regression models and random-effects meta-analysis were used to estimate hazard ratios (HRs) for type 2 diabetes.

    RESULTS

    In men, the HRs (95% CI) of type 2 diabetes were 1.40 (1.26, 1.55) for former smokers and 1.43 (1.27, 1.61) for current smokers, independent of age, education, center, physical activity, and alcohol, coffee, and meat consumption. In women, associations were weaker, with HRs (95% CI) of 1.18 (1.07, 1.30) and 1.13 (1.03, 1.25) for former and current smokers, respectively. There was some evidence of effect modification by BMI. The association tended to be slightly stronger in normal weight men compared with those with overall adiposity.

    CONCLUSIONS

    Former and current smoking was associated with a higher risk of incident type 2 diabetes compared with never smoking in men and women, independent of educational level, physical activity, alcohol consumption, and diet. Smoking may be regarded as a modifiable risk factor for type 2 diabetes, and smoking cessation should be encouraged for diabetes prevention.

  • 33.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Björ, Ove
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology. Onkologi.
    Ferrari, Pietro
    Nutrition and Hormones Group, International Agency for Research on Cancer-World Health Organization, Lyon, France.
    Lukanova, Annekatrin
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Lenner, Per
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology. Onkologi.
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Kaaks, Rudolf
    Division of Cancer Epidemiology, German Cancer Research Center Im Neuenheimer, Heidelberg, Germany.
    Prospective study of hyperglycemia and cancer risk.2007In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 30, no 3, p. 561-567Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To investigate whether hyperglycemia is associated with increased cancer risk.

    RESEARCH DESIGN AND METHODS: In the Västerbotten Intervention Project of northern Sweden, fasting and postload plasma glucose concentrations were available for 33,293 women and 31,304 men and 2,478 incident cases of cancer were identified. Relative risk (RR) of cancer for levels of fasting and postload glucose was calculated with the use of Poisson models, with adjustment for age, year of recruitment, fasting time, and smoking status. Repeated measurements 10 years after baseline in almost 10,000 subjects were used to correct RRs for random error in glucose measurements.

    RESULTS: Total cancer risk in women increased with rising plasma levels of fasting and postload glucose, up to an RR for the top versus bottom quartile of 1.26 (95% CI 1.09-1.47) (P(trend) <0.001) and 1.31 (1.12-1.52) (P(trend) = 0.001), respectively. Correction for random error in glucose measurements increased these risks up to 1.75 (1.32-2.36) and 1.63 (1.26-2.18), respectively. For men, corresponding uncorrected RR was 1.08 (0.92-1.27) (P(trend) = 0.25) and 0.98 (0.83-1.16) (P(trend) = 0.99), respectively. Risk of cancer of the pancreas, endometrium, urinary tract, and of malignant melanoma was statistically significantly associated with high fasting glucose with RRs of 2.49 (1.23-5.45) (P(trend) = 0.006), 1.86 (1.09-3.31) (P(trend) = 0.02), 1.69 (0.95-3.16) (P(trend) = 0.049), and 2.16 (1.14-4.35) (P(trend) = 0.01), respectively. Adjustment for BMI had no material effect on risk estimates.

    CONCLUSIONS: The association of hyperglycemia with total cancer risk in women and in women and men combined for several cancer sites, independently of obesity, provides further evidence for an association between abnormal glucose metabolism and cancer.

     

  • 34.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Lukanova, Annekatrin
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Kaaks, Rudolf
    Prospective study of hyperglycemia and cancer risk: Response to Bowker and Johnson2007In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 30, no 7, p. e78-Article in journal (Refereed)
  • 35. Sullivan, Shannon D.
    et al.
    Jablonski, Kathleen A.
    Florez, Jose C.
    Dabelea, Dana
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Dagogo-Jack, Sam
    Kim, Catherine
    Knowler, William C.
    Christophi, Costas A.
    Ratner, Robert
    Genetic Risk of Progression to Type 2 Diabetes and Response to Intensive Lifestyle or Metformin in Prediabetic Women With and Without a History of Gestational Diabetes Mellitus2014In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 37, no 4, p. 909-911Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE The Diabetes Prevention Program (DPP) trial investigated rates of progression to diabetes among adults with prediabetes randomized to treatment with placebo, metformin, or intensive lifestyle intervention. Among women in the DPP, diabetes risk reduction with metformin was greater in women with prior gestational diabetes mellitus (GDM) compared with women without GDM but with one or more previous live births. RESEARCH DESIGN AND METHODS We asked if genetic variability could account for these differences by comparing beta-cell function and genetic risk scores (GRS), calculated from 34 diabetes-associated loci, between women with and without histories of GDM. RESULTS beta-Cell function was reduced in women with GDM. The GRS was positively associated with a history of GDM; however, the GRS did not predict progression to diabetes or modulate response to intervention. CONCLUSIONS These data suggest that a diabetes-associated GRS is associated with development of GDM and may characterize women at risk for development of diabetes due to beta-cell dysfunction.

  • 36. van Nielen, Monique
    et al.
    Feskens, Edith J. M.
    Mensink, Marco
    Sluijs, Ivonne
    Molina, Esther
    Amiano, Pilar
    Ardanaz, Eva
    Balkau, Beverly
    Beulens, Joline W. J.
    Boeing, Heiner
    Clavel-Chapelon, Francoise
    Fagherazzi, Guy
    Franks, Paul W.
    Halkjaer, Jytte
    Maria Huerta, Jose
    Katzke, Verena
    Key, Timothy J.
    Khaw, Kay Tee
    Krogh, Vittorio
    Kuhn, Tilman
    Menendez, Virginia V. M.
    Nilsson, Peter
    Overvad, Kim
    Palli, Domenico
    Panico, Salvatore
    Rolandsson, Olov
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Romieu, Isabelle
    Sacerdote, Carlotta
    Sanchez, Maria-Jose
    Schulze, Matthias B.
    Spijkerman, Annemieke M. W.
    Tjonneland, Anne
    Tumino, Rosario
    Daphne, L. van der A.
    Wurtz, Anne M. L.
    Zamora-Ros, Raul
    Langenberg, Claudia
    Sharp, Stephen J.
    Forouhi, Nita G.
    Riboli, Elio
    Wareham, Nicholas J.
    Dietary Protein Intake and Incidence of Type 2 Diabetes in Europe: The EPIC-InterAct Case-Cohort Study2014In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 37, no 7, p. 1854-1862Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: The long-term association between dietary protein and type 2 diabetes incidence is uncertain. We aimed to investigate the association between total, animal, and plant protein intake and the incidence of type 2 diabetes. RESEARCH DESIGN AND METHODS: The prospective European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct case-cohort study consists of 12,403 incident type 2 diabetes cases and a stratified subcohort of 16,154 individuals from eight European countries, with an average follow-up time of 12.0 years. Pooled country-specific hazard ratios (HRs) and 95% CI of prentice-weighted Cox regression analyses were used to estimate type 2 diabetes incidence according to protein intake. RESULTS: After adjustment for important diabetes risk factors and dietary factors, the incidence of type 2 diabetes was higher in those with high intake of total protein (per 10 g: HR 1.06 [95% CI 1.02-1.09], P-trend < 0.001) and animal protein (per 10 g: 1.05 [1.02-1.08], P-trend = 0.001). Effect modification by sex (P < 0.001) and BMI among women (P < 0.001) was observed. Compared with the overall analyses, associations were stronger in women, more specifically obese women with a BMI > 30 kg/m(2) (per 10 g animal protein: 1.19 [1.09-1.32]), and nonsignificant in men. Plant protein intake was not associated with type 2 diabetes (per 10 g: 1.04 [0.93-1.16], P-trend = 0.098). CONCLUSIONS: High total and animal protein intake was associated with a modest elevated risk of type 2 diabetes in a large cohort of European adults. In view of the rapidly increasing prevalence of type 2 diabetes, limiting iso-energetic diets high in dietary proteins, particularly from animal sources, should be considered.

  • 37.
    Wennberg, Patrik
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Gustafsson, Per E
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Dunstan, David W
    Wennberg, Maria
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Hammarström, Anne
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Television viewing and low leisure-time physical activity in adolescence independently predict the metabolic syndrome in mid-adulthood2013In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 36, no 7, p. 2090-2097Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE We investigated whether television (TV) viewing and low leisure-time physical activity in adolescence predict the metabolic syndrome in mid-adulthood.

    RESEARCH DESIGN AND METHODS TV viewing habits and participation in leisure-time physical activity at age 16 years were assessed by self-administered questionnaires in a population-based cohort in Northern Sweden. The presence of the metabolic syndrome at age 43 years was ascertained in 888 participants (82% of the baseline sample) using the International Diabetes Federation criteria. Odds ratios (ORs) and CIs were calculated using logistic regression.

    RESULTS The overall prevalence of the metabolic syndrome at age 43 years was 26.9%. Adjusted OR for the metabolic syndrome at age 43 years was 2.14 (95% CI 1.24-3.71) for those who reported "watching several shows a day" versus "one show/week" or less and 2.31 (1.13-4.69) for leisure-time physical activity "several times/month" or less compared with "daily" leisure-time physical activity at age 16 years. TV viewing at age 16 years was associated with central obesity, low HDL cholesterol, and hypertension at age 43 years, whereas low leisure-time physical activity at age 16 years was associated with central obesity and triglycerides at age 43 years.

    CONCLUSIONS Both TV viewing and low leisure-time physical activity in adolescence independently predicted the metabolic syndrome and several of the metabolic syndrome components in mid-adulthood. These findings suggest that reduced TV viewing in adolescence, in addition to regular physical activity, may contribute to cardiometabolic health later in life.

  • 38. Zachrisson, I
    et al.
    Brismar, K
    Hall, K
    Wallensteen, M
    Dahlquist, Gisela
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Determinants of growth in diabetic pubertal subjects1997In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 20, no 8, p. 1261-1265Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To analyze the relationship among metabolic control, IGF-I, and growth in pubertal diabetic subjects.

    RESEARCH DESIGN AND METHODS: In 72 diabetic children, we have studied the pattern of change of IGF-I, IGF-I SD score, IGF binding protein (BP)-1, and growth rate in different pubertal stages and have analyzed their relation to age sex, weight/length index, HbA1c, insulin concentration, insulin dose, and dehydroepiandrosteronesulfate (DHEAS).

    RESULTS: The serum IGF-I values increased up to Tanner stage 4 and thereafter decreased, whereas IGFBP-1 showed the inverse pattern. When transforming the IGF-I values into SD scores, correcting for age, sex, and pubertal stage, it was shown that the deviation from normal values increased with increasing pubertal stage in boys, but was equal in stages 3-5 in girls. Using multiple regression analysis, HbA1c, insulin dose, and DHEAS were significantly correlated to IGF-I SD score (R2 = 0.253, P = 0.001). IGFBP-I levels in the afternoon were within normal range. LogIGFBP-1 showed an inverse correlation, to insulin concentration in single correlation (r = -0.26, P = 0.02). In single correlation, growth rate correlated significantly to insulin dose (r = 0.25, P = 0.03). In a multiple regression analysis, only DHEAS and IGF-I SD score were found to be significantly correlated to growth rate (R2 = 0.370, P < 0.001). The 18 adolescents who had reached their final height did not deviate from their target final height, according to their recorded growth since birth.

    CONCLUSIONS: In a group of fairly well-controlled diabetic children, the normal increase in IGF-I during puberty is blunted. Despite decreased IGF-I levels, target final height was attained, probably because of adequate insulin compensation leading to normal IGFBP-l, thus adequate bioavailability of IGF-I. Our results point out the importance of sufficient exogenous insulin in the period of rapid linear growth.

  • 39.
    Zhou, Kaixin
    et al.
    Division of Cardiovascular & Diabetes Medicine, Medical Research Institute, University of Dundee, Dundee, U.K..
    Donnelly, Louise A.
    Division of Cardiovascular & Diabetes Medicine, Medical Research Institute, University of Dundee, Dundee, U.K..
    Morris, Andrew D.
    Division of Cardiovascular & Diabetes Medicine, Medical Research Institute, University of Dundee, Dundee, U.K..
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Department of Clinical Science, Genetic & Molecular Epidemiology Unit, Lund University, Malmö, Sweden ; Department of Nutrition, Harvard University, School of Public Health, Boston, MA.
    Jennison, Chris
    Department of Mathematical Sciences, University of Bath, Bath, U.K..
    Palmer, Colin N. A.
    Division of Cardiovascular & Diabetes Medicine, Medical Research Institute, University of Dundee, Dundee, U.K..
    Pearson, Ewan R.
    Division of Cardiovascular & Diabetes Medicine, Medical Research Institute, University of Dundee, Dundee, U.K..
    Clinical and genetic determinants of progression of type 2 diabetes: a DIRECT study2014In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 37, no 3, p. 718-724Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To identify the clinical and genetic factors that explain why the rate of diabetes progression is highly variable between idividuals following diagnosis of type 2 diabetes.

    RESEARCH DESIGN AND METHODS: We studied 5,250 patients with type 2 diabetes using comprehensive electronic medical records in Tayside, Scotland, from 1992 onward. We investigated the association of clinical, biochemical, and genetic factors with the risk of progression of type 2 diabetes from diagnosis to the requirement of insulin treatment (defined as insulin treatment or HbA(1c) 8.5% [69 mmol/mol] treated with two or more noninsulin therapies).RESULTSRisk of progression was associated with both low and high BMI. In an analysis stratified by BMI and HbA(1c) at diagnosis, faster progression was independently associated with younger age at diagnosis, higher log triacylglyceride (TG) concentrations (hazard ratio [HR] 1.28 per mmol/L [95% CI 1.15-1.42]) and lower HDL concentrations (HR 0.70 per mmol/L [95% CI 0.55-0.87]). A high Genetic Risk Score derived from 61 diabetes risk variants was associated with a younger age at diagnosis and a younger age when starting insulin but was not associated with the progression rate from diabetes to the requirement of insulin treatment.

    CONCLUSIONS: Increased TG and low HDL levels are independently associated with increased rate of progression of diabetes. The genetic factors that predispose to diabetes are different from those that cause rapid progression of diabetes, suggesting a difference in biological process that needs further investigation.

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