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  • 1. Lindberg, Eva
    et al.
    Berne, C
    Franklin, Karl
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine.
    Svensson, Maria
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine.
    Janson, C
    Snoring and daytime sleepiness as risk factors for hypertension and diabetes in women--a population-based study.2007In: Respir Med, Vol. 101, no 6, p. 1283-90Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to analyze whether snoring and excessive daytime sleepiness (EDS), the main symptoms of obstructive sleep apnea syndrome (OSAS), are associated with hypertension and diabetes in women. A random sample of 6779 women aged 20-99 years answered questionnaires on sleep disturbances, daytime symptoms and somatic diseases. The women were categorized into four groups: "no EDS or snoring" (reference group), "snoring but no EDS", "EDS but no snoring" and "snoring and EDS". Prevalences of hypertension and diabetes were lowest in the reference group (8.7% and 1.6%, respectively) and highest among women with both snoring and EDS (hypertension: 26.3%, diabetes: 5.8%). In a multivariate model adjusting for age, body mass index, smoking, physical activity and alcohol dependency, "snoring and EDS" was a risk factor for hypertension (adjusted OR 1.82 (95% CI 1.30-2.55)) while isolated snoring or EDS was not. "Snoring and EDS" was more closely related to hypertension among women aged <50 years (adj. OR 3.41 (1.78-6.54) vs. 1.50 (1.02-2.19), P=0.01). For diabetes, both "EDS but no snoring" and "snoring and EDS" were risk factors and the associations were most pronounced in women aged >50 years (adj. OR 2.33 (1.28-4.26) for "EDS but no snoring" and 2.00 (1.05-3.84) for "snoring and EDS"). We conclude that the combination of snoring and EDS is a risk factor for hypertension and diabetes in women. For hypertension, the risk is partly age dependent and, for diabetes, EDS without snoring is a risk factor of similar magnitude. These differences might indicate differences in pathophysiologic mechanisms underlying the association between sleep-disordered breathing and hypertension and diabetes respectively.

  • 2.
    Lundgren, Magdalena
    et al.
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine.
    Svensson, Maria
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine.
    Lindmark, Stina
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine.
    Renström, Frida
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine.
    Ruge, Toralph
    Umeå University, Faculty of Medicine, Surgical and Perioperative Sciences, Surgery.
    Eriksson, Jan
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine.
    Fat cell enlargement is an independent marker of insulin resistance and 'hyperleptinaemia'.2007In: Diabetologia, ISSN 0012-186X, Vol. 50, no 3, p. 625-33Article in journal (Refereed)
  • 3.
    Möllsten, Anna
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Marklund, Stefan
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Wessman, Maija
    Svensson, Maria
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Forsblom, Carol
    Parkkonen, Maikki
    Brismar, Kerstin
    Groop, Per-Henrik
    Dahlquist, Gisela
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    A functional polymorphism in the manganese superoxide dismutase gene and diabetic nephropathy.2007In: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 56, no 1, p. 265-269Article in journal (Refereed)
    Abstract [en]

    Oxidative stress has been suggested to contribute to the development of diabetic nephropathy. Manganese superoxide dismutase (MnSOD) protects the cells from oxidative damage by scavenging free radicals. The demand for antioxidants is increased by smoking, which could disturb the balance between antioxidants and radicals. The present study aimed to determine whether a valine/alanine polymorphism in MnSOD (V16A, rs4880), alone or in combination with smoking, can contribute to development of diabetic nephropathy in 1,510 Finnish and Swedish patients with type 1 diabetes. Overt diabetic nephropathy (n = 619) was defined as having an albumin excretion rate (AER) >200 microg/min or renal replacement therapy; incipient diabetic nephropathy was defined as having an AER of 20-200 microg/min (n = 336). The control subjects had diabetes duration of >or=20 years, without albuminuria (AER <20 microg/min) and without antihypertensive treatment (n = 555). In addition to male sex and elevated A1C, smoking was significantly associated with diabetic nephropathy (overt plus incipient), odds ratio (OR) 2.00 (95% CI 1.60-2.50). When controlling for age at onset, diabetes duration, A1C, smoking, and sex, the Val/Val genotype was associated with an increase in risk of diabetic nephropathy (1.32 [1.00-1.74], P = 0.049). When evaluating the combined effect of genotype and smoking, we used logistic regression with stratification according to smoking status and genotype. The high-risk group (ever smoking plus Val/Val genotype) had 2.52 times increased risk of diabetic nephropathy (95% CI 1.73-3.69) compared with the low-risk group, but no departure from additivity was found. Our results indicate that smoking and homozygosity for the MnSOD Val allele is associated with an increased risk of diabetic nephropathy, which supports the hypothesis that oxidative stress contributes to the development of diabetic nephropathy.

  • 4.
    Möllsten, Anna
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Wessman, M
    Svensson, Maria
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Forsblom, C
    Parkkonen, M
    Brismar, K
    Groop, PH
    Dahlquist, Gisela
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Glu298Asp and NOS4ab polymorphisms in diabetic nephropathy.2006In: Annals of Medicine, ISSN 0785-3890, E-ISSN 1365-2060, Vol. 38, no 7, p. 522-528Article in journal (Other (popular science, discussion, etc.))
    Abstract [en]

    BACKGROUND AND AIMS: The risk of diabetic nephropathy (DN) increases with increase in intraglomerular pressure, which may partly be regulated by nitric oxide (NO). NO-production can be affected by polymorphisms in the endothelial NO-synthase gene (NOS3), hyperglycaemia and smoking. We therefore studied association between DN and two polymorphisms in NOS3, Glu298Asp and NOS4ab, in Caucasian type 1 diabetes (T1D) patients. PATIENTS AND METHODS: A total of 1510 Finnish and Swedish T1D patients were included in a cross-sectional case-control study. Incipient DN was defined as an albumin excretion rate (AER) of 20-200 microg/min (n = 336). Overt DN = AER>200 microg/min or renal replacement therapy (n = 619). All patients with DN were considered as cases. The controls were T1D patients with diabetes duration 20 years, AER<20 microg/min and without antihypertensive treatment (n = 555). The genetic markers studied were a 27 bp repeat (NOS4ab) and Glu298Asp (rs1799983). RESULTS: Age at onset of diabetes, male sex, duration of diabetes, HbA1c, blood pressure and smoking were assessed as possible confounders in the logistic regression analysis, which showed that homozygosity for the Glu-allele of the Glu298Asp-polymorphism was independently associated with increased risk of DN (OR = 1.46; 95% CI = 1.12-1.91). The variables smoking (OR = 2.13; 95% CI = 1.63-2.78), male sex (OR = 1.61; 95% CI = 1.23-2.10), HbA1c (OR per % increase above upper limit of the normal reference range = 1.02; 95% CI = 1.02-1.03), systolic (OR = 1.05; 95% CI = 1.04-1.06) and diastolic blood pressure (OR = 1.04; 95% CI = 1.02-1.05) also significantly and independently increased the risk of DN when taking age at diabetes onset and diabetes duration into account. The NOS4 a-allele was not associated with DN. CONCLUSIONS: The Glu/Glu-genotype of the NOS3 Glu298Asp polymorphism may increase the risk of developing DN independently of other known risk factors.

  • 5.
    Renström, Frida
    et al.
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine. Medicin.
    Buren, Jonas
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine. Medicin.
    Svensson, Maria
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine. Medicin.
    Eriksson, Jan
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine. Medicin.
    Insulin resistance induced by high glucose and high insulin precedes insulin receptor substrate 1 protein depletion in human adipocytes.2007In: Metabolism: Clinical and Experimental, ISSN 0026-0495, E-ISSN 1532-8600, Vol. 56, no 2, p. 190-198Article in journal (Refereed)
  • 6.
    Ruge, Toralph
    et al.
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry.
    Svensson, Maria
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Eriksson, Jan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Olivecrona, Gunilla
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry.
    Tissue-specific regulation of lipoprotein lipase in humans: effects of fasting.2005In: Eur J Clin Invest, ISSN 0014-2972, Vol. 35, no 3, p. 194-200Article in journal (Refereed)
  • 7. Sahli, David
    et al.
    Svensson, Maria
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine.
    Lidgren, Joakim
    Öjbrandt, K
    Eriksson, Jan
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine.
    Evaluation of simple non-invasive techniques for assessment of lower extremity arterial disease2005In: Clinical Physiology and Functional Imaging, ISSN 1475-0961, E-ISSN 1475-097X, Vol. 25, no 3, p. 129-134Article in journal (Refereed)
  • 8.
    Svensson, Maria
    et al.
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine.
    Eriksson, Jan
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine.
    Insulin resistance in diabetic nephropathy--cause or consequence?2006In: Diabetes Metab Res Rev, ISSN 1520-7552, Vol. 22, no 5, p. 401-10Article in journal (Refereed)
  • 9.
    Svensson, Maria
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Nyström, Lennarth
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Schön, S
    Dahlquist, G
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Age at onset of childhood-onset type 1 diabetes and the development of end-stage renal disease: a nationwide population-based study.2006In: Diabetes Care, Vol. 29, no 3, p. 538-42Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To analyze the impact of age at onset on the development of end-stage renal disease (ESRD) due to diabetic nephropathy in a nationwide population-based cohort with childhood-onset type 1 diabetes. RESEARCH DESIGN AND METHODS: A record linkage between two nationwide registers, the Swedish Childhood Diabetes Registry, including 12,032 cases with childhood-onset diabetes, and the Swedish Registry for Active Treatment of Uraemia was performed. Log-rank test was used to test differences between cumulative risk curves of developing ESRD due to diabetic nephropathy in three different strata of age at onset (0-4, 5-9, and 10-14 years). RESULTS: At a maximum follow-up of 27 years, 33 patients had developed ESRD due to diabetic nephropathy and all had a diabetes duration >15 years. In total, 4,414 patients had diabetes duration >15 years, and thus the risk in this cohort to develop ESRD was 33 of 4,414 (0.7%). A significant difference in risk of developing ESRD was found between the youngest (0-4 years) and the two older (5-9 and 10-14 years) age-at-onset strata (P = 0.03 and P = 0.001, respectively). A significant difference in the risk of developing ESRD was also found between children with prepubertal (0-4 and 5-9 years, n = 2,424) and pubertal (10-14 years, n = 2000) onset of diabetes (P = 0.002). No patient with onset of diabetes before 5 years of age had developed ESRD. CONCLUSIONS: With a median duration of 21 years in this population-based Swedish cohort with childhood-onset diabetes, <1% of the patients had developed ESRD due to diabetic nephropathy, and a prepubertal onset of diabetes seems to prolong the time to development of ESRD.

1 - 9 of 9
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