Pancreas · 2026
Effects of Glucagon-Like Peptide 1, Glucagon, and Glucose-Dependent Insulinotropic Polypeptide on Fluid Secretion in Guinea-Pig Pancreatic Duct Cells.
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Furuhashi-Higuchi Mayuko, Yamamoto Akiko, Fujiki Kotoyo, Nakakuki Miyuki, Taniguchi Itsuka, Nomura Nao, Liu Libin, Kozawa Yuka, Niwa Erina, Sato Suzuna, Yamaguchi Makoto, Ishiguro Hiroshi
Аннотация
OBJECTIVES: We examined the direct effects of glucagon-like peptide 1 (GLP-1), glucagon, and glucose-dependent insulinotropic polypeptide (GIP) on the physiological function of pancreatic duct cells by using interlobular duct segments isolated from the guinea-pig pancreas.
METHODS: The rate of fluid secretion was continuously measured by monitoring the luminal volume of isolated duct segments. cAMP production was measured in individual ducts by ELISA. Messenger RNA expression of GLP-1, glucagon, and GIP receptors in pancreatic duct cells was examined by quantitative reverse transcriptase-polymerase chain reaction.
RESULTS: All of GLP-1, glucagon, and GIP concentration-dependently stimulated fluid secretion. While the potency of GLP-1 was equivalent to that of secretin in physiological (10 and 30 pM) to pharmacological concentrations, higher concentrations (over 100 pM) of GIP were required for significant stimulation. The potency of glucagon was relatively weak. While GLP-1 and secretin additively stimulated fluid secretion, GIP and secretin synergistically stimulated fluid secretion when physiological concentrations were applied. In contrast, glucagon inhibited secretin-stimulated fluid secretion in a competitive manner. GLP-1 (1 nM) significantly increased cAMP production in isolated pancreatic ducts. Messenger RNA expression of GLP-1, glucagon, and GIP receptors was detected in isolated ducts. GLP-1 receptor immunoreactivity was detected in epithelial cells of pancreatic ducts.
CONCLUSIONS: Physiological concentrations of GLP-1 and GIP directly stimulate pancreatic duct fluid secretion by elevation of intracellular cAMP and interact with secretin in the guinea-pig. The physiological role of glucagon in the regulation of pancreatic duct fluid secretion is limited.
METHODS: The rate of fluid secretion was continuously measured by monitoring the luminal volume of isolated duct segments. cAMP production was measured in individual ducts by ELISA. Messenger RNA expression of GLP-1, glucagon, and GIP receptors in pancreatic duct cells was examined by quantitative reverse transcriptase-polymerase chain reaction.
RESULTS: All of GLP-1, glucagon, and GIP concentration-dependently stimulated fluid secretion. While the potency of GLP-1 was equivalent to that of secretin in physiological (10 and 30 pM) to pharmacological concentrations, higher concentrations (over 100 pM) of GIP were required for significant stimulation. The potency of glucagon was relatively weak. While GLP-1 and secretin additively stimulated fluid secretion, GIP and secretin synergistically stimulated fluid secretion when physiological concentrations were applied. In contrast, glucagon inhibited secretin-stimulated fluid secretion in a competitive manner. GLP-1 (1 nM) significantly increased cAMP production in isolated pancreatic ducts. Messenger RNA expression of GLP-1, glucagon, and GIP receptors was detected in isolated ducts. GLP-1 receptor immunoreactivity was detected in epithelial cells of pancreatic ducts.
CONCLUSIONS: Physiological concentrations of GLP-1 and GIP directly stimulate pancreatic duct fluid secretion by elevation of intracellular cAMP and interact with secretin in the guinea-pig. The physiological role of glucagon in the regulation of pancreatic duct fluid secretion is limited.