Gut microbial markers are associated with diabetes onset, regulatory imbalance, and IFN-γ level in NOD Mice

Krych, Łukasz; Nielsen, Dennis Sandris; Hansen, Axel Kornerup; Hansen, Camilla Hartmann Friis

doi:10.1080/19490976.2015.1011876

Cited by 116 publications

(113 citation statements)

References 36 publications

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“…Association of Bacteroides with diabetes development in different animal models of T1D is less clear. In one study, Bacteroides spp were found to be more abundant in young NOD mice which did not develop diabetes 33. In this study, Bacteroides spp abundance associated with low-diabetes incidence and revealed the presence of species potentially supporting the establishment of immune tolerance in the NOD/MrkTac colony, such as B. fragilis and B. thetaiotaomicron 13 14 17 18 (see also online supplementary discussion).…”

Section: Discussionmentioning

confidence: 53%

Akkermansia muciniphila induces gut microbiota remodelling and controls islet autoimmunity in NOD mice

Hänninen

Toivonen

Pöysti

et al. 2017

Gut

299

211

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Section: Discussionmentioning

confidence: 53%

Akkermansia muciniphila induces gut microbiota remodelling and controls islet autoimmunity in NOD mice

Hänninen

Toivonen

Pöysti

et al. 2017

Gut

299

211

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“…One relative abundance difference was that S24-7 decreased in the Ex (p<0.05) but not the WM (p=0.2) group. This species has been shown to differ between diabetic and non-diabetic mice (19); thus, this Ex-related shift may be in line with the robust insulin-sensitizing effect of exercise. Opposite to previous observations reported by Kang et al, we observed an increase in the relative abundance of Streptococcus with exercise (17).…”

Section: Discussionmentioning

confidence: 69%

Comparison of Diet versus Exercise on Metabolic Function and Gut Microbiota in Obese Rats

Welly

Liu

Zidon

et al. 2016

Medicine &Amp; Science in Sports &Amp; Exercise

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Cardiometabolic impairments that begin early in life are particularly critical, as they often predict metabolic dysfunction into adulthood. Obesity, high-fat diet (HFD), and inactivity are all associated with adipose tissue (AT) inflammation and insulin resistance (IR), major predictors of metabolic dysfunction. Recent evidence also has associated the gut microbiome with cardiometabolic health. PURPOSE Compare equal energy deficits induced by exercise and caloric reduction on cardiometabolic disease risk parameters including AT inflammation, IR and gut microbiota changes during HFD consumption. METHODS Obesity-prone rats fed HFD were exercise trained (Ex, n=10) or weight-matched to Ex via caloric reduction while kept sedentary (WM, n=10), and compared to ad libitum HFD-fed (Sed, n=10) rats for IR, systemic energetics and spontaneous physical activity (SPA), adiposity, and fasting metabolic parameters. Visceral, subcutaneous, periaortic, and brown AT, liver, aorta, and cecal digesta were examined. RESULTS Despite identical reductions in adiposity, Ex, but not WM, improved IR, increased SPA by ~26% (p<0.05 compared to WM and Sed), and reduced LDL cholesterol (p<0.05 compared to Sed). WM and Ex both reduced inflammatory markers in all AT depots and aorta, while only Ex increased indicators of mitochondrial function in brown AT. Ex significantly increased the relative abundance of cecal Streptococcaceae and decreased S24-7 and one undefined genus in Rikenellacea; WM induced similar changes that did not reach statistical significance. CONCLUSIONS Both Ex and WM reduced AT inflammation across depots, while Ex caused more robust changes to gut microbial communities, improved IR, increased fat oxidation, increased SPA, and increased indices of brown AT mitochondrial function. Our findings add to the growing body of literature indicating that there are weight-loss independent metabolic benefits of exercise.

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“…The intestinal microbiomes of Eα16/NOD mice showed increased α-diversity, which has been associated with protection from T1D in genetically susceptible mice and humans (25,26). To directly confirm this conclusion, we compared the ability of intestinal microbiota from Eα16/NOD vs. NOD donors to protect NOD recipients from insulitis.…”

Section: Eα16/nod Mice Hosted a Distinct Intestinal Microbiome Early Inmentioning

confidence: 99%

Protective major histocompatibility complex allele prevents type 1 diabetes by shaping the intestinal microbiota early in ontogeny

Silverman

Kua

Tanca

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Certain MHC-II or HLA-D alleles dominantly protect from particular autoimmune diseases. For example, expression of the MHC-II Eα:Eβ complex potently protects nonobese diabetic (NOD) mice, which normally lack this isotype, from spontaneous development of type 1 diabetes. However, the underlying mechanisms remain debated. We investigated MHC-II–mediated protection from type 1 diabetes using a previously reported NOD mouse line expressing an Eα transgene and, thereby, the Eα:Eβ complex. Eα16/NOD females vertically protected their NOD offspring from diabetes and insulitis, an effect that was dependent on the intestinal microbiota; moreover, they developed autoimmunity when treated with certain antibiotics or raised in a germ-free environment. Genomic and proteomic analyses revealed NOD and Eα16/NOD mice to host mild but significant differences in the intestinal microbiotas during a critical early window of ontogeny, and transfer of cecal contents from the latter to the former suppressed insulitis. Thus, protection from autoimmunity afforded by particular MHC/HLA alleles can operate via intestinal microbes, highlighting potentially important societal implications of treating infants, or even just their pregnant mothers, with antibiotics.

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Gut microbial markers are associated with diabetes onset, regulatory imbalance, and IFN-γ level in NOD Mice

Cited by 116 publications

References 36 publications

Akkermansia muciniphila induces gut microbiota remodelling and controls islet autoimmunity in NOD mice

Akkermansia muciniphila induces gut microbiota remodelling and controls islet autoimmunity in NOD mice

Comparison of Diet versus Exercise on Metabolic Function and Gut Microbiota in Obese Rats

Protective major histocompatibility complex allele prevents type 1 diabetes by shaping the intestinal microbiota early in ontogeny

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