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  • 1
    Publication Date: 2014-03-29
    Description: Bariatric surgical procedures, such as vertical sleeve gastrectomy (VSG), are at present the most effective therapy for the treatment of obesity, and are associated with considerable improvements in co-morbidities, including type-2 diabetes mellitus. The underlying molecular mechanisms contributing to these benefits remain largely undetermined, despite offering the potential to reveal new targets for therapeutic intervention. Substantial changes in circulating total bile acids are known to occur after VSG. Moreover, bile acids are known to regulate metabolism by binding to the nuclear receptor FXR (farsenoid-X receptor, also known as NR1H4). We therefore examined the results of VSG surgery applied to mice with diet-induced obesity and targeted genetic disruption of FXR. Here we demonstrate that the therapeutic value of VSG does not result from mechanical restriction imposed by a smaller stomach. Rather, VSG is associated with increased circulating bile acids, and associated changes to gut microbial communities. Moreover, in the absence of FXR, the ability of VSG to reduce body weight and improve glucose tolerance is substantially reduced. These results point to bile acids and FXR signalling as an important molecular underpinning for the beneficial effects of this weight-loss surgery.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4016120/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4016120/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryan, Karen K -- Tremaroli, Valentina -- Clemmensen, Christoffer -- Kovatcheva-Datchary, Petia -- Myronovych, Andriy -- Karns, Rebekah -- Wilson-Perez, Hilary E -- Sandoval, Darleen A -- Kohli, Rohit -- Backhed, Fredrik -- Seeley, Randy J -- DK078392/DK/NIDDK NIH HHS/ -- DK082173/DK/NIDDK NIH HHS/ -- DK093848/DK/NIDDK NIH HHS/ -- HL111319/HL/NHLBI NIH HHS/ -- K08 DK084310/DK/NIDDK NIH HHS/ -- K99 HL111319/HL/NHLBI NIH HHS/ -- P30 DK078392/DK/NIDDK NIH HHS/ -- England -- Nature. 2014 May 8;509(7499):183-8. doi: 10.1038/nature13135. Epub 2014 Mar 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Cincinnati, Cincinnati, Ohio 45237, USA. ; Wallenberg Laboratory, Department of Molecular and Clinical Medicine and Sahlgrenska Center for Cardiovascular and Metabolic Research, University of Gothenburg, S-413 45 Gothenburg, Sweden. ; 1] Department of Internal Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Cincinnati, Cincinnati, Ohio 45237, USA [2] Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Universitetsparken 2, DK-2100 Copenhagen, Denmark. ; Department of Pediatrics, Division of Gastroenterology, Hepatology, and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA. ; Divison of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA. ; 1] Wallenberg Laboratory, Department of Molecular and Clinical Medicine and Sahlgrenska Center for Cardiovascular and Metabolic Research, University of Gothenburg, S-413 45 Gothenburg, Sweden [2] Novo Nordisk Foundation Center for Basic Metabolic Research, Section for Metabolic Receptology and Enteroendocrinology, Faculty of Health Sciences, University of Copenhagen, Copenhagen, DK-2200, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670636" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bariatric Surgery ; Bile Acids and Salts/blood ; Body Composition ; Cecum/microbiology ; Feeding Behavior ; *Gastrectomy ; Glucose Intolerance/surgery ; Glucose Tolerance Test ; Male ; Mice ; Mice, Inbred C57BL ; Obesity/etiology/surgery ; Receptors, Cytoplasmic and Nuclear/deficiency/genetics/*metabolism ; Signal Transduction ; Stomach/metabolism/surgery ; Weight Loss
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2013-05-31
    Description: Type 2 diabetes (T2D) is a result of complex gene-environment interactions, and several risk factors have been identified, including age, family history, diet, sedentary lifestyle and obesity. Statistical models that combine known risk factors for T2D can partly identify individuals at high risk of developing the disease. However, these studies have so far indicated that human genetics contributes little to the models, whereas socio-demographic and environmental factors have greater influence. Recent evidence suggests the importance of the gut microbiota as an environmental factor, and an altered gut microbiota has been linked to metabolic diseases including obesity, diabetes and cardiovascular disease. Here we use shotgun sequencing to characterize the faecal metagenome of 145 European women with normal, impaired or diabetic glucose control. We observe compositional and functional alterations in the metagenomes of women with T2D, and develop a mathematical model based on metagenomic profiles that identified T2D with high accuracy. We applied this model to women with impaired glucose tolerance, and show that it can identify women who have a diabetes-like metabolism. Furthermore, glucose control and medication were unlikely to have major confounding effects. We also applied our model to a recently described Chinese cohort and show that the discriminant metagenomic markers for T2D differ between the European and Chinese cohorts. Therefore, metagenomic predictive tools for T2D should be specific for the age and geographical location of the populations studied.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karlsson, Fredrik H -- Tremaroli, Valentina -- Nookaew, Intawat -- Bergstrom, Goran -- Behre, Carl Johan -- Fagerberg, Bjorn -- Nielsen, Jens -- Backhed, Fredrik -- England -- Nature. 2013 Jun 6;498(7452):99-103. doi: 10.1038/nature12198. Epub 2013 May 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical and Biological Engineering, Chalmers University of Technology, SE-412 96 Gothenburg, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23719380" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Aged ; Asian Continental Ancestry Group ; Bacteria/genetics/isolation & purification ; Biomarkers ; Blood Glucose/*metabolism ; Cluster Analysis ; Cohort Studies ; Confounding Factors (Epidemiology) ; Demography ; Diabetes Mellitus, Type 2/blood/drug therapy/genetics/*microbiology ; Environment ; European Continental Ancestry Group ; Feces/microbiology ; Female ; Gastrointestinal Tract/*microbiology ; Glucose Intolerance/blood/metabolism/*microbiology ; *Health ; Humans ; *Metagenome/genetics ; Middle Aged ; Models, Biological ; Prognosis ; Species Specificity ; Sweden
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2012-09-14
    Description: The link between the microbes in the human gut and the development of obesity, cardiovascular disease and metabolic syndromes, such as type 2 diabetes, is becoming clearer. However, because of the complexity of the microbial community, the functional connections are less well understood. Studies in both mice and humans are helping to show what effect the gut microbiota has on host metabolism by improving energy yield from food and modulating dietary or the host-derived compounds that alter host metabolic pathways. Through increased knowledge of the mechanisms involved in the interactions between the microbiota and its host, we will be in a better position to develop treatments for metabolic disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tremaroli, Valentina -- Backhed, Fredrik -- England -- Nature. 2012 Sep 13;489(7415):242-9. doi: 10.1038/nature11552.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wallenberg Laboratory for Cardiovascular and Metabolic Research, Sahlgrenska University Hospital, 413 45 Gothenburg, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22972297" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diet ; *Energy Metabolism ; Fermentation ; Humans ; Immunity, Innate ; Inflammation/metabolism/microbiology ; Intestines/immunology/*metabolism/*microbiology ; Metabolic Syndrome X/metabolism/microbiology ; Metagenome/immunology/*physiology ; Obesity/metabolism/microbiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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