The role of gastric function in control of food intake (and body weight) in relation to obesity, as well as pharmacological and surgical interventions

Abstract

PurposeThe objectives of this review are to summarize the role of gastric motor functions in the development of satiation (defined broadly as postprandial fullness) and satiety (reduced appetite or postponing desire to eat after a meal) and their impact on weight change. The specific topics are the methods of measurement of gastric emptying and accommodation and their impact on food intake, satiation, and satiety. A second focus contrasts bariatric surgery to endoscopic gastroplasty that alter gastric emptying and incretin responses in markedly divergent manners.BackgroundThe hormone, GLP‐1, retards gastric emptying and increases gastric accommodation through vagally‐mediated effects. Indeed, these effects provide the basis for the association of altered gastric emptying in the appetite and weight loss responses to pharmacological interventions particularly by those acting on receptors of incretin agonists such as liraglutide and the dual agonists, tirzepatide and cotadutide, all of which retard gastric emptying. In fact, retardation of gastric emptying and gastrointestinal adverse effects have been shown to contribute in part to the weight loss in response to this class of pharmacological agents.SummaryThe motor functions of the stomach are relevant to postprandial fullness and to interventions aimed at weight loss in people with obesity.

Rikkunshito increases peripheral incretin-hormone levels in humans and rats

“…Incretin hormones are also GI hormones and have received significant attention because of their important roles in glucose homeostasis, type 2 diabetes, and potentially other metabolic disorders[ 12 ]. Glucose intake leads to a stimulation of insulin secretion than an intravenous administration of glucose[ 13 ]. This is known as the incretin effect, which is attributed to the fact that oral glucose intake leads to the release of incretin hormones, including gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), from entero-endocrine cells in the gastrointestinal tract.…”

“…This is known as the incretin effect, which is attributed to the fact that oral glucose intake leads to the release of incretin hormones, including gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), from entero-endocrine cells in the gastrointestinal tract. In contrast, intravenous glucose administration does not induce the release of incretin hormones[ 13 ]. The GI hormones released in response to nutrient absorption act as endocrine signals to the pancreatic islet cells, augmenting insulin secretion.…”

Newer pharmacological interventions directed at gut hormones for obesity

“…Several recently published reviews have addressed particularly the impressive metabolic effects of the gut hormone co-agonists (Nogueiras et al, 2023). With increased recognition of the role of gastric function in appetite and food intake, and their modulation by pharmacological and bariatric interventions (Camilleri, 2023), this review incorporates a focus on the pharmacological effects of approved and experimental agents for obesity on gastric emptying to complement established effects on appetite.…”

Editorial overview

“…Along with the important roles of aforementioned critical peptides in appetite and weight regulation, motility disorders of the gut remain or newly emerge as highly prevalent clinical problems subsequent to pharmacological and surgical treatment of obesity [8][9][10]. Gala et al (pp.…”

“…Gala et al (pp. 131–137) expertly introduce the broad range of GI peptides that are affected by metabolic and bariatric surgery through various mechanisms and could represent targets for potential new pharmacological treatment options to improve gut motility disorders [10–12].…”