Lack of Effect of Synthetic Human Gastric Inhibitory Polypeptide and Glucagon-LikePeptide 1 [7-36 Amide] Infused at Near-Physiological Concentrations on Pentagastrin-Stimulated Gastric Acid Secretion in Normal Human Subjects

Abstract

Gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 [7-36 amide] (GLP-1) are glucose-dependent insulinotropic gut hormones. Under experimental conditions, both have been shown to reduce stimulated gastric acid secretion. To study their individual and combined effects on pentagastrin-stimulated (0.1 μg/kg/h from – 90 to 120 min) gastric volume, acid and chloride output, on separate occasions, synthetic human GIP (1 pmol/kg/min) and/or GLP-1 [7-36 amide] (0.3 pmol/ kg/min) or placebo (0.9% NaCl with 1 % albumin) were infused intravenously (from – 30 to 120 min) in 9 healthy volunteers. At 0 min, a glucose infusion was started that mimicked the glycemic profile after an oral glucose load of 50 g/400 ml and allowed for the glucose-dependent insulinotropic action of GIP and GLP-1 [7-36 amide]. Pentagastrin stimulated acid output significantly, but neither GIP nor GLP-1 [7-36 amide] either alone or in combination, reduced pentagastrin-stimulated gastric acid secretion. The circulating concentrations of GIP and GLP-1 [7-36 amide] obtained at steady state during exogenous administration of synthetic peptides were similar to or higher than those reached after oral glucose (endogenous secretion). In conclusion, (penta) gastrin-stimulated gastric acid secretion is not inhibited by physiological circulating concentrations of GIP or GLP-1 [7-36 amide]. Therefore, the insulinotropic action of these intestinal hormones is physiologically more important than their possible role as enterogastrone.

Gastric inhibitory polypeptide and effects of glycation on glucose transport and metabolism in isolated mouse abdominal muscle

“…GIP can inhibit gastric acid secretion in man but only at supra-physiological concentrations (Maxwell et al 1980, Nauck et al 1992. However, GIP has a number of other potentially important actions which mirror some of the effects of insulin.…”

Relating Food Emulsion Structure and Composition to the Way It Is Processed in the Gastrointestinal Tract and Physiological Responses: What Are the Opportunities?

“…At higher levels, glucose-dependent insulinotropic peptide (GIP, formerly named gastric inhibitory peptide), secreted by the endocrine K cells in the duodenum and jejunum, also down-regulates the secretion of gastrin and through this inhibits acid secretion, but this only occurs at physiologically unachievable high GIP levels. 77 Nutrient sensing by the intestinal mucosa induces inhibitory signals, which are sent to nuclei of the vagus nerve, leading to a down-regulation of stomach activity and stomach emptying. The inhibitory reflex is obtained for all three macronutrients (carbohydrate, protein, and fat).…”

Hiperplasia adrenal macronodular independente de ACTH (AIMAH): aspectos clínicos e moleculares

“…O GIP exerce seu efeito através da ligação a seu receptor específico, o GIPR (26), que é expresso em vários tecidos humanos. Em adição ao seu efeito insulinotrópico já bem caracterizado, o GIP via GIPR possui outros efeitos fisiológi-cos, como a regulação da secreção de ácidos no estôma-go, regulação da circulação esplâncnica, estimulação da lipogênese em adipócitos e modulação da função dos osteoblastos (27)(28)(29). Por outro lado, investiga-se a possibilidade de a presença de anormalidades no GIP-GIPR estar envolvida na etiopatogênese de doenças como d i abetes mellitus tipo 2 e obesidade (30)(31)(32).…”