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Understanding Bile Acid Signaling in Diabetes: From Pathophysiology to Therapeutic Targets |
Jessica M. Ferrell and John Y. L. Chiang  |
Integrative Medical Sciences, Northeast Ohio Medical University, Rootstown, OH, USA. |
Corresponding author: John Y. L. Chiang. Integrative Medical Sciences Northeast Ohio Medical University, SR44, PO Box 95 Rootstown, OH 44272, USA. Email: jchiang@neomed.edu
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Received March 06, 2019; Accepted April 25, 2019.
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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Abstract
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Diabetes and obesity have reached an epidemic status worldwide. Diabetes increases the risk for cardiovascular disease and non-alcoholic fatty liver disease. Primary bile acids are synthesized in hepatocytes and are transformed to secondary bile acids in the intestine by gut bacteria. Bile acids are nutrient sensors and metabolic integrators that regulate lipid, glucose, and energy homeostasis by activating nuclear farnesoid X receptor and membrane Takeda G protein-coupled receptor 5. Bile acids control gut bacteria overgrowth, species population, and protect the integrity of the intestinal barrier. Gut bacteria, in turn, control circulating bile acid composition and pool size. Dysregulation of bile acid homeostasis and dysbiosis causes diabetes and obesity. Targeting bile acid signaling and the gut microbiome have therapeutic potential for treating diabetes, obesity, and non-alcoholic fatty liver disease.
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Keywords:
Bile acids and salts; Gastrointestinal microbiome; Non-alcoholic fatty liver disease; Receptors, cytoplasmic and nuclear; Receptors, G-protein-coupled
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