Improved glucose metabolism following bariatric surgery is associated with increased circulating bile acid concentrations and remodeling of the gut microbiome.
Clinical studies have indicated that circulating bile acid (BA) concentrations increase following bariatric surgery, especially following malabsorptive procedures such as Roux-en-Y gastric bypasses (RYGB). Moreover, total circulating BA concentrations in patients following RYGB are positively correlated with serum glucagon-like peptide-1 concentrations and inversely correlated with postprandial glucose concentrations. Overall, these data suggest that the increased circulating BA concentrations following bariatric surgery - independently of calorie restriction and body-weight loss - could contribute, at least in part, to improvements in insulin sensitivity, incretin hormone secretion, and postprandial glycemia, leading to the remission of type-2 diabetes (T2DM). In humans, the primary and secondary BA pool size is dependent on the rate of biosynthesis and the enterohepatic circulation of BAs, as well as on the gut microbiota, which play a crucial role in BA biotransformation. Moreover, BAs and gut microbiota are closely integrated and affect each other. Thus, the alterations in bile flow that result from anatomical changes caused by bariatric surgery and changes in gut microbiome may influence circulating BA concentrations and could subsequently contribute to T2DM remission following RYGB. Research data coming largely from animal and cell culture models suggest that BAs can contribute,vianuclear farnezoid X receptor (FXR) and membrane G-protein-receptor (TGR-5), to beneficial effects on glucose metabolism. It is therefore likely that FXR, TGR-5, and BAs play a similar role in glucose metabolism following bariatric surgery in humans. The objective of this review is to discuss in detail the results of published studies that show how bariatric surgery affects glucose metabolism and subsequently T2DM remission.
Lukasz Kaska, General, Endocrine and Transplant Surgery, Medical University of Gdańsk, 80-214 Gdańsk, Poland.
Lukasz
L
Kaska
Lukasz Kaska, General, Endocrine and Transplant Surgery, Medical University of Gdańsk, 80-214 Gdańsk, Poland.
Tomasz
T
Sledzinski
Lukasz Kaska, General, Endocrine and Transplant Surgery, Medical University of Gdańsk, 80-214 Gdańsk, Poland.
Agnieszka
A
Chomiczewska
Lukasz Kaska, General, Endocrine and Transplant Surgery, Medical University of Gdańsk, 80-214 Gdańsk, Poland.
Agnieszka
A
Dettlaff-Pokora
Lukasz Kaska, General, Endocrine and Transplant Surgery, Medical University of Gdańsk, 80-214 Gdańsk, Poland.
Julian
J
Swierczynski
D050110:Bariatric Surgery / Q000379:methods*; D001647:Bile Acids and Salts / Q000737:chemistry*; D031204:Caloric Restriction; D003924:Diabetes Mellitus, Type 2 / Q000473:pathology; D015390:Gastric Bypass; D000069196:Gastrointestinal Microbiome; D041981:Gastrointestinal Tract / Q000473:pathology; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008099:Liver / Q000473:pathology; D010100:Oxygen / Q000737:chemistry; D010455:Peptides / Q000737:chemistry; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D012074:Remission Induction; D000099150:Receptor, Farnesoid X-Activated
D001647:Bile Acids and Salts; D005947:Glucose; D010100:Oxygen; D010455:Peptides; D018160:Receptors, Cytoplasmic and Nuclear; D043562:Receptors, G-Protein-Coupled; D000099150:Receptor, Farnesoid X-Activated; C473772:GPBAR1 protein, human
Bariatric surgery; Bile acids; Gut microbiota; RXR; Roux-en-Y gastric bypasses; TGR-5; Type-2 diabetes