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Bile acids and gut peptide secretion after bariatric surgery: A 1‐year prospective randomized pilot trial
Author(s) -
Steinert Robert E.,
Peterli Ralph,
Keller Sylvia,
MeyerGerspach Anne C.,
Drewe Jürgen,
Peters Thomas,
Beglinger Christoph
Publication year - 2013
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.20522
Subject(s) - medicine , postprandial , sleeve gastrectomy , glycemic , basal (medicine) , gastroenterology , peptide yy , prospective cohort study , randomized controlled trial , gastric bypass surgery , meal , bile acid , surgery , endocrinology , gastric bypass , weight loss , obesity , insulin , receptor , neuropeptide , neuropeptide y receptor
Objective Increased delivery of bile acid salts (BA) to distal L‐cells and altered TGR5 receptor activation may contribute to the early and substantial increases in gut peptide secretion seen after bariatric surgery. To further elucidate a potential role of BA in the secretion of GLP‐1 and PYY, we analyzed plasma BA concentrations in 14 morbidly obese patients undergoing gastric bypass or sleeve gastrectomy in a prospective, randomized 1‐year trial. Design and Methods Patients received a standard test meal and blood was collected before and after eating, prior to, and 1 week, 3 months, and 12 months after surgery. Results Pre‐surgery, basal BA concentrations were significantly lower in bariatric patients than in healthy controls. One year post‐surgery, bariatric patients expressed variably increased BA concentrations (gastric bypass patients ∼2 fold increase, P ≤ 0.05). However, whereas in both patient groups, marked increases in GLP‐1 and PYY and improved glycemic control was seen already 1 week and 3 months post‐surgery, changes in plasma BA followed a different pattern: basal and postprandial plasma BA concentrations increased much slower, more progressively with significant increases only 1‐year post‐surgery. Conclusions Based on these findings, BA do not appear to be key mediators of the early increase in GLP‐1 and PYY response in post‐bariatric patients.