Bile acids and bariatric surgery.

Albaugh VL, Banan B, Ajouz H, Abumrad NN, Flynn CR
Mol Aspects Med. 2017 56: 75-89

PMID: 28390813 · PMCID: PMC5603298 · DOI:10.1016/j.mam.2017.04.001

Bariatric surgery, specifically Roux-en-Y gastric bypass (RYGB) and vertical sleeve gastrectomy (VSG), are the most effective and durable treatments for morbid obesity and potentially a viable treatment for type 2 diabetes (T2D). The resolution rate of T2D following these procedures is between 40 and 80% and far surpasses that achieved by medical management alone. The molecular basis for this improvement is not entirely understood, but has been attributed in part to the altered enterohepatic circulation of bile acids. In this review we highlight how bile acids potentially contribute to improved lipid and glucose homeostasis, insulin sensitivity and energy expenditure after these procedures. The impact of altered bile acid levels in enterohepatic circulation is also associated with changes in gut microflora, which may further contribute to some of these beneficial effects. We highlight the beneficial effects of experimental surgical procedures in rodents that alter bile secretory flow without gastric restriction or altering nutrient flow. This information suggests a role for bile acids beyond dietary fat emulsification in altering whole body glucose and lipid metabolism strongly, and also suggests emerging roles for the activation of the bile acid receptors farnesoid x receptor (FXR) and G-protein coupled bile acid receptor (TGR5) in these improvements. The limitations of rodent studies and the current state of our understanding is reviewed and the potential effects of bile acids mediating the short- and long-term metabolic improvements after bariatric surgery is critically examined.

Copyright © 2017 Elsevier Ltd. All rights reserved.

MeSH Terms (17)

Animals Bile Acids and Salts Diabetes Mellitus, Type 2 Enterohepatic Circulation Gastrectomy Gastric Bypass Gastrointestinal Microbiome Gene Expression Regulation Glucose Homeostasis Humans Insulin Resistance Obesity, Morbid Receptors, Cytoplasmic and Nuclear Receptors, G-Protein-Coupled Rodentia Signal Transduction

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