Mechanisms in bariatric surgery: Gut hormones, diabetes resolution, and weight loss

TY - JOUR

T1 - Mechanisms in bariatric surgery

T2 - Gut hormones, diabetes resolution, and weight loss

AU - Holst, Jens Juul

AU - Madsbad, Sten

AU - Bojsen-Møller, Kirstine N

AU - Svane, Maria Saur

AU - Jørgensen, Nils Bruun

AU - Dirksen, Carsten

AU - Martinussen, Christoffer

N1 - Copyright © 2018 American Society for Bariatric Surgery. Published by Elsevier Inc. All rights reserved.

PY - 2018/5

Y1 - 2018/5

N2 - Gastric bypass surgery leads to profound changes in the secretion of gut hormones with effects on metabolism, appetite, and food intake. Here, we discuss their contributions to the improvement in glucose tolerance and the weight loss that results from the operations. We find that the improved glucose tolerance is due the following events: a negative energy balance and resulting weight loss, which improve first hepatic and later peripheral insulin sensitivity, in combination with increased postprandial insulin secretion elicited particularly by exaggerated glucagon-like peptide-1 responses. The weight loss is due to loss of appetite resulting in reduced energy intake, and we find it probable that this process is driven by exaggerated secretion of appetite-regulating gut hormones including, but probably not limited to, glucagon-like peptide-1 and peptide-YY. The increased secretion is due to an accelerated exposure to and absorption of nutrients in the small intestine. This places the weight loss and the gut hormones in key positions with respect to the metabolic improvements after bypass surgery.

AB - Gastric bypass surgery leads to profound changes in the secretion of gut hormones with effects on metabolism, appetite, and food intake. Here, we discuss their contributions to the improvement in glucose tolerance and the weight loss that results from the operations. We find that the improved glucose tolerance is due the following events: a negative energy balance and resulting weight loss, which improve first hepatic and later peripheral insulin sensitivity, in combination with increased postprandial insulin secretion elicited particularly by exaggerated glucagon-like peptide-1 responses. The weight loss is due to loss of appetite resulting in reduced energy intake, and we find it probable that this process is driven by exaggerated secretion of appetite-regulating gut hormones including, but probably not limited to, glucagon-like peptide-1 and peptide-YY. The increased secretion is due to an accelerated exposure to and absorption of nutrients in the small intestine. This places the weight loss and the gut hormones in key positions with respect to the metabolic improvements after bypass surgery.

KW - Appetite/physiology

KW - Bariatric Surgery

KW - Diabetes Mellitus, Type 2/surgery

KW - Dietary Carbohydrates/metabolism

KW - Dietary Proteins/metabolism

KW - Digestion/physiology

KW - Eating/physiology

KW - Gastric Bypass

KW - Gastrointestinal Hormones/physiology

KW - Glucagon-Like Peptide 1/physiology

KW - Humans

KW - Insulin Resistance/physiology

KW - Intestinal Absorption/physiology

KW - Nutrients/metabolism

KW - Obesity, Morbid/complications

KW - Peptide YY/physiology

KW - Weight Loss/physiology

U2 - 10.1016/j.soard.2018.03.003

DO - 10.1016/j.soard.2018.03.003

M3 - Journal article

C2 - 29776493

SN - 1550-7289

VL - 14

SP - 708

EP - 714

JO - Surgery for Obesity and Related Diseases

JF - Surgery for Obesity and Related Diseases

IS - 5

ER -