Journal
JOURNAL OF DIABETES RESEARCH
Volume 2018, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2018/3462092
Keywords
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Funding
- Wake Forest School of Medicine
- Center on Diabetes, Obesity, and Metabolism
- Department of Defense [PR170446]
- Wake Forest Clinical and Translational Science Institute (WF CTSI) - National Center for Advancing Translational Sciences (NCATS), National Institutes of Health [UL1TR001420]
- NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES [UL1TR001420] Funding Source: NIH RePORTER
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This study aimed to determine the association between non-high-fat diet-induced obesity- (non-DIO-) associated gut microbiome dysbiosis with gut abnormalities like cellular turnover of intestinal cells, tight junctions, and mucin formation that can impact gut permeability. We used leptin-deficient (Lep(ob/ob)) mice in comparison to C57BL/6J control mice, which are fed on identical diets, and performed comparative and correlative analyses of gut microbiome composition, gut permeability, intestinal structural changes, tight junction-mucin formation, cellular turnover, and sternness genes. We found that obesity impacted cellular turnover of the intestine with increased cell death and cell survival/proliferation gene expression with enhanced stemness, which are associated with increased intestinal permeability, changes in villi/crypt length, and decreased expression of tight junctions and mucus synthesis genes along with dysbiotic gut microbiome signature. Obesity-induced gut microbiome dysbiosis is also associated with abnormal intestinal organoid formation characterized with decreased budding and higher stemness. Results suggest that non-DIO-associated gut microbiome dysbiosis is associated with changes in the intestinal cell death versus cell proliferation homeostasis and functions to control tight junctions and mucous synthesis-regulating gut permeability.
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