Postprandial Glucagon-like Peptide-1 Secretion Research Articles

Inhibition of insulin, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) secretion by octreotide has no effect on post-heparin plasma lipoprotein lipase activity.

This study examines the immediate effect of modulating postprandial insulin and insulinotropic hormone (glucose-dependent insulinotropic polypeptide, GIP; glucagon-like peptide-1, GLP-1) secretion on the activation of lipoprotein lipase (LPL) in six lean and six obese age-matched women. Subjects were given, on two separate occasions, 340 kcal of carbohydrate alone or combined with an IV infusion of octreotide, (100 microg infusion from 30 min before the meal for 150 min). Post-heparin LPL activity (10,000 U) was measured on each occasion 120 minutes post-carbohydrate. Following oral carbohydrate postprandial plasma insulin levels were significantly higher in obese subjects than in lean (p < 0.01). Glucose tolerance was slightly impaired in obese subjects. Insulin, GIP and GLP-1 secretion post-carbohydrate was markedly reduced by octreotide in lean and obese subjects. LPL activity was similar in the two groups after carbohydrate administration and was unaffected by octreotide. Inhibition of postprandial insulin, GIP and GLP-1 secretion acutely did not reduce post-heparin LPL activity either in lean or obese subjects.

Dietary fiber modulates intestinal proglucagon messenger ribonucleic acid and postprandial secretion of glucagon-like peptide-1 and insulin in rats

Dietary fiber modulates intestinal proglucagon messenger ribonucleic acid and postprandial secretion of glucagon-like peptide-1 and insulin in rats

Galanin is a potent inhibitor of glucagon-like peptide-1 secretion from rat ileum.

The insulinotropic glucagon-like peptide 1 (GLP-1) originates from the lower intestines. Surprisingly, food ingestion induces a rapid increase of GLP-1 plasma levels. Therefore, a complex regulation for postprandial GLP-1 secretion must exist, which cannot be solely explained by direct contact of nutrients in the gut lumen with the GLP-1-releasing L cells. This was addressed in the present study utilizing an isolated vascularly perfused rat ileum preparation. Cholinergic (methacholine) as well as peptidergic stimulation by glucose-dependent insulin-releasing polypeptide (synonym: gastric inhibitory polypeptide) (GIP) strongly enhanced GLP-1 secretion from the rat ileum. The stimulation of GLP-1 secretion by methacholine was abolished by addition of atropine and partly reduced by galanin. Galanin dose-dependently antagonized the stimulatory effect of GIP on GLP-1 release. Atropine was without effect. Furthermore, employing double immunohistochemistry labeling techniques galanin-immunoreactive nerves were detected in the vicinity of GLP-1-immunostained cells. Our data indicate that stimulatory and inhibitory mediators regulate GLP-1 secretion and that galanin is a likely inhibitor.

Regulation of glucagon-like peptide-1 secretion from rat ileum by neurotransmitters and peptides.

Food ingestion induces a rapid increase in the insulinotropic glucagon-like peptide-1 (GLP-1) in plasma. Paradoxically, GLP-1 originates from the lower intestines and therefore a complex regulation of postprandial GLP-1 secretion must exist. This was addressed in the present study by utilizing an isolated vascularly perfused rat ileum preparation. Peptides and neurotransmitters thought to be candidate mediators triggering GLP-1 secretion were arterially infused and GLP-1 was measured in the venous effluent. Arterial infusion of cholinergic agonists strongly enhanced GLP-1 secretion which was counteracted by the addition of atropine. Histamine, dopamine, 5-hydoxytryptamine, gamma-aminobutyric acid, and norepinephrine had no effect. Peptides of the bombesin family were strong stimulants whereas tachykinins, enkephalins, dynorphin, TRH, calcitonin-gene-related peptide and members of the secretin family, vasoactive intestinal peptide, peptide histidine isoleucine and neuropeptide Y, were less effective. The second incretin hormone, gastric inhibitory polypeptide (GIP), was the most potent stimulant of GLP-1 secretion in our study. It enhanced GLP-1 release up to sixfold above basal during the early phase followed by a sustained secretion at 400% above basal. This stimulation remained unaffected by atropine. In conclusion, in addition to luminal stimulation of nutrients, a cholinergic impulse as well as peptidergic mediators (among them possibly GIP and GRP) may have an impact on postprandial GLP-1 secretion from the rat ileum.