Umeå University's logo

umu.sePublications
Change search
Link to record
Permanent link

Direct link
Sjödin, Kotryna SimonyteORCID iD iconorcid.org/0000-0002-1323-9913
Alternative names
Publications (10 of 18) Show all publications
Sjödin, K. S., Sjödin, A., Ruszczyński, M., Kristensen, M. B., Hernell, O., Szajewska, H. & West, C. E. (2023). Targeting the gut-lung axis by synbiotic feeding to infants in a randomized controlled trial. BMC Biology, 21(1), Article ID 38.
Open this publication in new window or tab >>Targeting the gut-lung axis by synbiotic feeding to infants in a randomized controlled trial
Show others...
2023 (English)In: BMC Biology, E-ISSN 1741-7007, Vol. 21, no 1, article id 38Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Formula-fed infants are at increased risk of infections. Due to the cross-talk between the mucosal systems of the gastrointestinal and respiratory tracts, adding synbiotics (prebiotics and probiotics) to infant formula may prevent infections even at distant sites. Infants that were born full term and weaned from breast milk were randomized to prebiotic formula (fructo- and galactooligosaccharides) or the same prebiotic formula with Lactobacillus paracasei ssp. paracasei F19 (synbiotics) from 1 to 6 months of age. The objective was to examine the synbiotic effects on gut microbiota development. RESULTS: Fecal samples collected at ages 1, 4, 6, and 12 months were analyzed using 16S rRNA gene sequencing and a combination of untargeted gas chromatography-mass spectrometry/liquid chromatography-mass spectrometry. These analyses revealed that the synbiotic group had a lower abundance of Klebsiella, a higher abundance of Bifidobacterium breve compared to the prebiotic group, and increases in the anti-microbial metabolite d-3-phenyllactic acid. We also analyzed the fecal metagenome and antibiotic resistome in the 11 infants that had been diagnosed with lower respiratory tract infection (cases) and 11 matched controls using deep metagenomic sequencing. Cases with lower respiratory tract infection had a higher abundance of Klebsiella species and antimicrobial resistance genes related to Klebsiella pneumoniae, compared to controls. The results obtained using 16S rRNA gene amplicon and metagenomic sequencing were confirmed in silico by successful recovery of the metagenome-assembled genomes of the bacteria of interest. CONCLUSIONS: This study demonstrates the additional benefit of feeding specific synbiotics to formula-fed infants over prebiotics only. Synbiotic feeding led to the underrepresentation of Klebsiella, enrichment of bifidobacteria, and increases in microbial degradation metabolites implicated in immune signaling and in the gut-lung and gut-skin axes. Our findings support future clinical evaluation of synbiotic formula in the prevention of infections and associated antibiotic treatment as a primary outcome when breastfeeding is not feasible. TRIAL REGISTRATION: ClinicalTrials.gov NCT01625273. Retrospectively registered on 21 June 2012.

Place, publisher, year, edition, pages
BioMed Central (BMC), 2023
Keywords
Antibiotics, Bifidobacteria, Infant gut microbiota, Klebsiella, Lower respiratory tract infection, Prebiotics, Probiotics
National Category
Nutrition and Dietetics Pediatrics
Identifiers
urn:nbn:se:umu:diva-205355 (URN)10.1186/s12915-023-01531-3 (DOI)000936843800002 ()36803508 (PubMedID)2-s2.0-85148399778 (Scopus ID)
Funder
Umeå UniversityRegion VästerbottenMagnus Bergvall FoundationKnut and Alice Wallenberg FoundationSwedish Research Council
Available from: 2023-04-03 Created: 2023-04-03 Last updated: 2024-01-17Bibliographically approved
Bzioueche, H., Sjödin, K. S., West, C. E., Khemis, A., Rocchi, S., Passeron, T. & Tulic, M. K. (2021). Analysis of Matched Skin and Gut Microbiome of Patients with Vitiligo Reveals Deep Skin Dysbiosis: Link with Mitochondrial and Immune Changes. Journal of Investigative Dermatology, 141(9), 2280-2290
Open this publication in new window or tab >>Analysis of Matched Skin and Gut Microbiome of Patients with Vitiligo Reveals Deep Skin Dysbiosis: Link with Mitochondrial and Immune Changes
Show others...
2021 (English)In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 141, no 9, p. 2280-2290Article in journal (Refereed) Published
Abstract [en]

Vitiligo is an autoimmune disease characterized by patchy, white skin owing to melanocyte loss. Commensal cutaneous or gut dysbiosis has been linked to various dermatological disorders. In this study, we studied the skin and gut microbiota of patients with vitiligo compared with those of healthy controls. We obtained swabs and biopsies from both lesional and nonlesional skin as well as stool and blood samples from each individual. We detected reduced richness and diversity of microbiota in the stools of subjects with vitiligo compared with the stools of the controls (P < 0.01). Skin swabs had greater α-diversity than biopsies (P < 0.001); swabs from lesional sites were primarily depleted of Staphylococcus compared with those from nonlesional sites (P < 0.02). Sampling deeper layers from the same patients showed differences in both α- and β-diversity between samples with decreased richness and distribution of species (P < 0.01) in the lesional site. Biopsy microbiota from the lesional skin had distinct microbiota composition, which was depleted of protective Bifidobacterium and Bacteroides but was enriched in Proteobacteria, Streptococcus, Mycoplasma, and mtDNA (P < 0.001); the latter increased in the same patients with heightened innate immunity and stress markers in their blood (P < 0.05). These data describe vitiligo-specific cutaneous and gut microbiota and a link between skin dysbiosis, mitochondrial damage, and immunity in patients with vitiligo.

Place, publisher, year, edition, pages
Elsevier, 2021
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:umu:diva-189892 (URN)10.1016/j.jid.2021.01.036 (DOI)000689355100138 ()33771527 (PubMedID)2-s2.0-85104986767 (Scopus ID)
Available from: 2021-11-24 Created: 2021-11-24 Last updated: 2023-03-23Bibliographically approved
Sjödin, K. S., Domellöf, M., Lagerqvist, C., Hernell, O., Lönnerdal, B., Szymlek-Gay, E. A., . . . Lind, T. (2019). Administration of ferrous sulfate drops has significant effects on the gut microbiota of iron-sufficient infants: a randomised controlled study [Letter to the editor]. Gut, 68(11)
Open this publication in new window or tab >>Administration of ferrous sulfate drops has significant effects on the gut microbiota of iron-sufficient infants: a randomised controlled study
Show others...
2019 (English)In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 68, no 11Article in journal, Letter (Refereed) Published
Place, publisher, year, edition, pages
BMJ Publishing Group Ltd, 2019
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:umu:diva-167039 (URN)10.1136/gutjnl-2018-316988 (DOI)000497817400023 ()30343273 (PubMedID)2-s2.0-85055356819 (Scopus ID)
Funder
Västerbotten County Council
Available from: 2020-01-09 Created: 2020-01-09 Last updated: 2023-03-24Bibliographically approved
Simonyté Sjödin, K., Hammarström, M.-L., Rydén, P., Sjödin, A., Hernell, O., Engstrand, L. & West, C. E. (2019). Temporal and long-term gut microbiota variation in allergic disease: a prospective study from infancy to school age. Allergy. European Journal of Allergy and Clinical Immunology, 74(1), 176-185
Open this publication in new window or tab >>Temporal and long-term gut microbiota variation in allergic disease: a prospective study from infancy to school age
Show others...
2019 (English)In: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 74, no 1, p. 176-185Article in journal (Refereed) Published
Abstract [en]

Background: Compositional changes in the early‐life gut microbiota have been implicated in IgE‐associated allergic diseases, but there is lack of longitudinal studies. We examined gut microbiota development from infancy to school age in relation to onset of IgE‐associated allergic diseases. At 8 years of age, we also examined the relationship between gut microbiota and T‐cell regulation, estimated as responses to polyclonal T‐cell activation.

Methods: Stool samples were collected from 93 children at 4, 6, 13 months, and 8 years of age. The gut microbiota was profiled using 16S rRNA gene sequencing. Peripheral blood was drawn from all children, and mononuclear cells were polyclonally activated. Levels of IL‐10 and FOXP3 mRNA copies were determined using real‐time quantitative reverse transcriptase‐PCR.

Results: At 8 years of age, 21 children were diagnosed with IgE‐associated allergic disease and 90% displayed allergic comorbidity. Seventy‐two children were nonallergic and nonsensitized. Statistical tests with multiple testing corrections demonstrated temporal underrepresentation of Ruminococcus and consistent underrepresentation of Bacteroides, Prevotella, and Coprococcus in allergic compared to nonallergic children from infancy to school age. The gut microbiota of the allergic 8‐year‐olds was enriched in Bifidobacteriumand depleted of Lactobacillus, Enterococcus, and Lachnospira. In allergic 8‐year-olds, Faecalibacterium correlated with IL‐10 mRNA levels (rs = 0.49, Padj = 0.02) with the same trend for FOXP3 (rs = 0.39, Padj = 0.08).

Conclusions: We identified both temporal and long‐term variation in the differential abundance of specific bacterial genera in children developing IgE‐associated allergic disease. Improved dietary interventions aiming at expanding immune‐modulatory taxa could be studied for prevention of allergic disease.

Place, publisher, year, edition, pages
John Wiley & Sons, 2019
Keywords
allergy, diversity, intestinal colonization, microbiome, T-cell response
National Category
Immunology in the medical area
Identifiers
urn:nbn:se:umu:diva-157612 (URN)10.1111/all.13485 (DOI)000459664100017 ()29786876 (PubMedID)2-s2.0-85055285542 (Scopus ID)
Available from: 2019-03-27 Created: 2019-03-27 Last updated: 2023-03-24Bibliographically approved
Sjödin, K. S., Vidman, L., Rydén, P. & West, C. E. (2016). Emerging evidence of the role of gut microbiota in the development of allergic diseases. Current Opinion in Allergy and Clinical Immunology, 16(4), 390-395
Open this publication in new window or tab >>Emerging evidence of the role of gut microbiota in the development of allergic diseases
2016 (English)In: Current Opinion in Allergy and Clinical Immunology, ISSN 1528-4050, E-ISSN 1473-6322, Vol. 16, no 4, p. 390-395Article, review/survey (Refereed) Published
Abstract [en]

Purpose of review The purpose is to review recent studies examining the role of gut microbiota in allergic diseases and asthma.

Recent findings Work in experimental models gives further evidence that a disturbed gut microbiota influences the propensity to develop allergic manifestations, and that changing the gut microbiota by dietary means (high fiber/acetate or prebiotics) in pregnancy may reduce the risk of allergic airways disease and food allergy in the offspring, respectively. The gut microbiome in established allergic disease and prior to disease onset has also been assessed in clinical trials. One study demonstrated a strong association between high abundance of Faecalibacterium prausnitzii and decreased levels of butyrate and propionate, and established eczema. Lower relative abundance of Ruminococcaceae appears to be implicated in food sensitization and to precede the development of atopic eczema. Decreased relative abundance of Lachnospira, Veillonella, Faecalibacterium, and Rothia in early infancy was reported to be associated with increased asthma risk. Inoculation of germ-free mice with these genera decreased airway inflammation in their offspring thereby proposing a causal role of bacteria in preventing allergic airways disease.

Summary Gut microbiome research is an actively developing field. Although candidate bacterial taxa have been reported it still remains unclear which bacteria (or other microbes), in which numbers and combinations, and when during the gut colonization process may prevent allergic diseases and asthma. There is still a call for standardized approaches that will enable direct comparison of different studies.

Keywords
allergic disease, asthma, biodiversity, gut microbiome, homeostasis, immunity
National Category
Immunology in the medical area Respiratory Medicine and Allergy
Identifiers
urn:nbn:se:umu:diva-124315 (URN)10.1097/ACI.0000000000000277 (DOI)000379587800015 ()2-s2.0-84973163312 (Scopus ID)
External cooperation:
Available from: 2016-09-06 Created: 2016-08-04 Last updated: 2023-03-24Bibliographically approved
Stomby, A., Simonyte, K., Mellberg, C., Ryberg, M., Stimson, R. H., Larsson, C., . . . Olsson, T. (2015). Diet-induced weight loss has chronic tissue-specific effects on glucocorticoid metabolism in overweight postmenopausal women. International Journal of Obesity, 39(5), 814-819
Open this publication in new window or tab >>Diet-induced weight loss has chronic tissue-specific effects on glucocorticoid metabolism in overweight postmenopausal women
Show others...
2015 (English)In: International Journal of Obesity, ISSN 0307-0565, E-ISSN 1476-5497, Vol. 39, no 5, p. 814-819Article in journal (Refereed) Published
Abstract [en]

Background/Objectives: Tissue-specific glucocorticoid metabolism is altered in obesity, and may increase cardiovascular risk. This dysregulation is normalized by short-term calorie restriction and weight loss, an effect that varies with dietary macronutrient composition. However, tissue-specific glucocorticoid metabolism has not been studied during long-term (>6 months) dietary interventions. Therefore our aim was to test whether long-term dietary interventions, either a paleolithic-type diet (PD) or a diet according to Nordic nutrition recommendations (NNR) could normalize tissue-specific glucocorticoid metabolism in overweight and obese women.

Subjects/Methods: Forty-nine overweight/obese postmenopausal women were randomized to a paleolithic diet or a diet according to NNR for 24 months. At baseline, 6 and 24 months anthropometric measurements, insulin sensitivity, excretion of urinary glucocorticoid metabolites in 24-hour collections, conversion of orally administered cortisone to plasma cortisol and transcript levels of 11β hydroxysteroid dehydrogenase type 1 (11βHSD1) in subcutaneous adipose tissue were studied.

Results: Both diet groups achieved significant and sustained weight loss. Weight loss with the PD was greater than on NNR diet after 6 months (P<0.001) but similar at 24 months. Urinary measurement of 5α-reductase activity was increased after 24 months in both groups compared with baseline (P<0.001). Subcutaneous adipose tissue 11βHSD1 gene expression decreased at 6 and 24 months in both diet groups (P=0.036). Consistent with increased liver 11βHSD1, conversion of oral cortisone to cortisol increased at 6 months (P=0.023) but was unchanged compared with baseline by 24 months.

Conclusions: Long-term weight loss in postmenopausal women has tissue-specific and time-dependent effects on glucocorticoid metabolism. This may alter local-tissue cortisol exposure contributing to improved metabolic function during weight loss.

National Category
Nutrition and Dietetics
Identifiers
urn:nbn:se:umu:diva-96782 (URN)10.1038/ijo.2014.188 (DOI)000354097900013 ()25349058 (PubMedID)2-s2.0-84928924061 (Scopus ID)
Available from: 2014-12-03 Created: 2014-12-03 Last updated: 2023-03-24Bibliographically approved
Rojo, M. L., Cipriano, M., Söderstrom, I., Simonyte, K., Olsson, T. & Fowler, C. J. (2014). Effects of dietary glucose and fructose upon cannabinoid CB1 receptor functionality in the rat brain: a pilot study. Life Sciences, 108(2), 116-121
Open this publication in new window or tab >>Effects of dietary glucose and fructose upon cannabinoid CB1 receptor functionality in the rat brain: a pilot study
Show others...
2014 (English)In: Life Sciences, ISSN 0024-3205, E-ISSN 1879-0631, Vol. 108, no 2, p. 116-121Article in journal (Refereed) Published
Abstract [en]

Aims: A high consumption of fructose leads not only to peripheral changes in insulin sensitivity and vascular function, but also to central changes in several brain regions. Given the role of the endogenous cannabinoid system in the control of energy intake, we undertook a pilot study to determine whether a high fructose diet produced changes in brain CB1 receptor functionality. Main methods: Male rats given access ad libitum to normal chow were given either water, glucose or fructose solutions to drink. CBI receptor functionality was measured autoradiographically as the increase in [35SJGTP)/S binding produced by the agonist CP55,940. Key findings: Seven regions were investigated: the prefrontal cortex, caudate-putamen, hippocampal CAI-CA3, dentate gyrus, amygdala, and dorsomedial and ventromedial hypothalami. Two-way robust Wilcoxon analyses for each brain region indicated that the dietary treatment did not produce significant main effects upon agonist-stimulated [35S]GThyS binding in any of the regions, in contrast to a significant main effect upon both leptin and adiponectin levels in the blood. However, a MANCOVA of the data controlling for leptin and adiponectin as co-variables identified a significant effect of glucose and fructose treatment for five weeks upon the [35S]GTPI/S response in the ventromedial hypothalamus, a region of importance for regulation of appetite. Significance: It is concluded from this pilot study that palatable solutions do not produce overt changes in brain CBI receptor functionality, although subtle changes in discrete brain regions may occur.

Place, publisher, year, edition, pages
Elsevier, 2014
Keywords
Fructose, Endocannabinoid, fructose, endocannabinoid, CB1 receptors, [S-35]GTP gamma S autoradiography, leptin, adiponectin
National Category
Pharmaceutical Sciences
Identifiers
urn:nbn:se:umu:diva-91832 (URN)10.1016/j.lfs.2014.05.019 (DOI)000339367100008 ()2-s2.0-84903903745 (Scopus ID)
Available from: 2014-09-01 Created: 2014-08-18 Last updated: 2023-03-24Bibliographically approved
Rask, E., Simonyte, K., Lönn, L. & Axelson, M. (2013). Cortisol metabolism after weight loss: associations with 11 beta-HSD type 1 and markers of obesity in women. Clinical Endocrinology, 78(5), 700-705
Open this publication in new window or tab >>Cortisol metabolism after weight loss: associations with 11 beta-HSD type 1 and markers of obesity in women
2013 (English)In: Clinical Endocrinology, ISSN 0300-0664, E-ISSN 1365-2265, Vol. 78, no 5, p. 700-705Article in journal (Refereed) Published
Abstract [en]

Objective Increased glucocorticoid metabolite excretion and enhanced expression and activity of 11-hydroxysteroid dehydrogenase type 1 in adipose tissue are closely correlated with obesity and its detrimental consequences. Weight loss ameliorates the latter. The aim of this study was to explore whether increased glucocorticoid exposure in obesity is improved with substantial weight loss and thus is a consequence rather than a cause of obesity. Design and patients A prospective cohort study in 31 women. Measurements 11-HSD type 1 expression and activity, urinary glucocorticoid metabolite excretion, body composition including regional adipose tissue depots and insulin resistance by HOMA-IR before and 2years after gastric bypass surgery. Results After weight loss, excretion of cortisol and cortisone metabolites decreased. Both cortisol and cortisone metabolite excretion correlated with central obesity, where the intraabdominal fat depot showed the strongest association. Cortisol metabolites correlated with 11-HSD type 1 activity in abdominal subcutaneous adipose tissue. The ratio of cortisol to cortisone metabolites [(5-tetrahydrocortisol (5THF)+tetrahydrocortisol (THF)+-cortol)/(tetrahydrocortisone (THE)+-cortolone)] and the ratio of 5-THF/THF both decreased after stable weight loss, reflecting a downregulation of the net activities of 11-HSD type 1 and 5-reductase. Conclusion Long-term weight loss in women is not only followed by reduced glucocorticoid production, but also favourably decreases the global and tissue-specific activity of the cortisol-activating enzyme 11 -HSD type 1, possibly contributing to the health benefits of bariatric surgery.

National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:umu:diva-71078 (URN)10.1111/j.1365-2265.2012.04333.x (DOI)000317615300010 ()2-s2.0-84876143836 (Scopus ID)
Available from: 2013-06-17 Created: 2013-05-20 Last updated: 2023-03-24Bibliographically approved
Alvehus, M., Simonyte, K., Andersson, T., Söderström, I., Burén, J., Rask, E., . . . Olsson, T. (2012). Adipose tissue IL-8 is increased in normal weight women after menopause and reduced after gastric bypass surgery in obese women. Clinical Endocrinology, 77(5), 684-690
Open this publication in new window or tab >>Adipose tissue IL-8 is increased in normal weight women after menopause and reduced after gastric bypass surgery in obese women
Show others...
2012 (English)In: Clinical Endocrinology, ISSN 0300-0664, E-ISSN 1365-2265, Vol. 77, no 5, p. 684-690Article in journal (Refereed) Published
Abstract [en]

Objective:  The menopausal transition is characterized by increased body fat accumulation, including redistribution from peripheral to central fat depots. This distribution is associated with an increased risk of type 2 diabetes and cardiovascular disease which are linked to low-grade inflammation. We determined whether postmenopausal women have higher levels of inflammatory markers, compared to premenopausal women. We also wanted to determine if these markers are reduced by stable weight loss in obese women. Design and methods:  Anthropometric data, blood samples, and subcutaneous adipose tissue biopsies were collected from normal weight premenopausal and postmenopausal women and obese women before and 2 years after gastric bypass surgery. Serum protein levels and adipose tissue gene expression of inflammatory markers were investigated. Results:  IL-8 expression in adipose tissue and circulating levels were higher in postmenopausal versus premenopausal women. IL-8 expression was associated with waist circumference, independent of menopausal status. IL-6 expression and serum levels of monocyte chemoattractant protein (MCP)-1 were higher in postmenopausal versus premenopausal women. Two years after gastric bypass surgery, adipose expression of IL-8, tumor necrosis factor-α, and MCP-1 decreased significantly. Serum insulin levels were associated with inflammation-related gene expression before gastric bypass surgery, but these associations disappeared after surgery. Conclusion:  Postmenopausal women have an increased inflammatory response in the subcutaneous fat and circulation. Inflammatory markers in adipose tissue decreased significantly after surgery-induced weight loss. This effect may be beneficial for metabolic control and reduced cardiovascular risk after weight loss. © 2011 Blackwell Publishing Ltd.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2012
Keywords
IL-8, menopause, gastric bypass surgery
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:umu:diva-51103 (URN)10.1111/j.1365-2265.2011.04322.x (DOI)22168600 (PubMedID)2-s2.0-84867255274 (Scopus ID)
Available from: 2012-01-10 Created: 2012-01-10 Last updated: 2023-03-24Bibliographically approved
McInnes, K. J., Andersson, T. C., Simonyte, K., Söderström, I., Mattsson, C., Seckl, J. R. & Olsson, T. (2012). Association of 11 beta-hydroxysteroid dehydrogenase type I expression and activity with estrogen receptor beta in adipose tissue from postmenopausal women. Menopause: The Journal of the North American Menopause, 19(12), 1347-1352
Open this publication in new window or tab >>Association of 11 beta-hydroxysteroid dehydrogenase type I expression and activity with estrogen receptor beta in adipose tissue from postmenopausal women
Show others...
2012 (English)In: Menopause: The Journal of the North American Menopause, ISSN 1072-3714, E-ISSN 1530-0374, Vol. 19, no 12, p. 1347-1352Article in journal (Refereed) Published
Abstract [en]

Objective: 11 beta-Hydroxysteroid dehydrogenase type I (11 beta HSD1) regenerates active cortisol from inert cortisone in adipose tissue. Elevated adipose tissue 11 beta HSD1 activity is observed in obese humans and rodents, where it is linked to obesity and its metabolic consequences. Menopause is also associated with increased abdominal fat accumulation, suggesting that estrogen is also important in adipose tissue metabolism. The purpose of this current study was to establish whether estrogen signaling through estrogen receptor alpha (ER-alpha) and estrogen receptor beta (ER-beta) could influence 11 beta HSD1 in premenopausal and postmenopausal adipose tissues. Methods: Nineteen premenopausal (aged 26 +/- 5 y; body mass index, 23.6 +/- 1.6 kg/m(2)) and 23 postmenopausal (aged 63 +/- 4 y; body mass index, 23.4 +/- 1.9 kg/m(2)) healthy women were studied. Subcutaneous adipose tissue biopsies and fasting venous blood samples were taken. Body composition was measured by bioelectrical impedance analysis. Human Simpson-Golabi-Behmel syndrome adipocyte cells were treated with ER-alpha- and ER-beta-specific agonists for 24 hours. Basic anthropometric data, serum 17 beta-estradiol and progesterone concentrations, ER-alpha and ER-beta messenger RNA (mRNA) levels, and 11 beta HSD1 mRNA, protein, and activity levels were assessed. Results: ER-beta and 11 beta HSD1, but not ER-alpha, mRNAs were significantly increased in adipose tissue from postmenopausal women compared with premenopausal women. ER-beta had a significant positive correlation with the mRNA level of 11 beta HSD1 in adipose tissue from premenopausal and postmenopausal women. This association between ER-beta and 11 beta HSD1 was greatest in adipose tissue from postmenopausal women. In human Simpson-Golabi-Behmel syndrome adipocytes, diarylpropiolnitrile, a selective ER-beta agonist, increased 11 beta HSD1 mRNA, protein, and activity levels. Conclusions: We conclude that, in adipose tissue, ER-beta-mediated estrogen signaling can up-regulate 11 beta HSD1 and that this may be of particular importance in postmenopausal women.

Keywords
Menopause, Estrogen receptor beta, 11 beta-Hydroxysteroid dehydrogenase type I, Adipose tissue
National Category
Obstetrics, Gynecology and Reproductive Medicine
Identifiers
urn:nbn:se:umu:diva-63018 (URN)10.1097/gme.0b013e318258aad7 (DOI)000311830800011 ()2-s2.0-84871241652 (Scopus ID)
Available from: 2013-01-02 Created: 2012-12-27 Last updated: 2023-03-24Bibliographically approved
Projects
Nicotinamide N-methyltransferase (NNMT) in obesity and type 2 diabetes [2012-06616_VR]; Umeå University
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-1323-9913

Search in DiVA

Show all publications