GLP-1-(7-36) amide, -(1-37), and -(1-36) amide: potent cAMP-dependent stimuli of rat parietal cell function

Schmidtler, J.; Schepp, Wolfgang; Janczewska, I; Weigert, N.; Furlinger, C.; Schusdziarra, V.; Classen, Meinhard

doi:10.1152/ajpgi.1991.260.6.g940

Cited by 20 publications

(21 citation statements)

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“…It was well-known that GLP-1 was one of the most potent factors for the enhancement of insulin secretion, and there were a few papers suggesting that GCG may increase insulin secretion by improving b-cell function with EC 50 at about 10 pM (Schmidtler et al 1991, Fehmann et al 1995. Our study showed that BBR treatment may increase GLP-1(7-36) amide release in plasma and intestine, the concentration of GCG in portal vein blood was about 30 pM, this suggested that BBR may improve b-cell function and tissue insulin via enhancing GCG release.…”

Section: Discussionmentioning

confidence: 99%

Berberine promotes glucagon-like peptide-1 (7–36) amide secretion in streptozotocin-induced diabetic rats

Lu¹,

Yu²,

Zhu³

et al. 2008

Journal of Endocrinology

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Berberine (BBR), a hypoglycemic agent, has shown beneficial metabolic effects for anti-diabetes, but its precise mechanism was unclear. Glucagon-like peptide-1 (GLP-1) is considered to be an important incretin that can decrease hyperglycemia in the gastrointestinal tract after meals. The aim of this study was to investigate whether BBR exerts its anti-diabetic effects via modulating GCG secretion. Diabeteslike rats induced by streptozotocin received BBR (120 mg/kg per day, i.g) for 5 weeks. Two hours following the last dose, the rats were anaesthetized and received 2 . 5 g/kg glucose by gavage. At 15-minute and 30-minute after glucose load, blood samples, pancreas, and intestines were obtained to measure insulin and GCG using ELISA kit. The number of L cells in the ileum and b-cells in the pancreas were identified using immunohistology. The expression of proglucagon mRNA in the ileum was measured by RT-PCR. The results indicated that BBR treatment significantly increased GCG levels in plasma and intestine (P!0 . 05) accompanied with the increase of proglucagon mRNA expression and the number of L-cell compared with the controls (P!0 . 05).Furthermore, BBR increased insulin levels in plasma and pancreas as well as b-cell number in pancreas. The data support the hypothesis that the anti-diabetic effects of BBR may partly result from enhancing GCG secretion.

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Section: Discussionmentioning

confidence: 99%

Berberine promotes glucagon-like peptide-1 (7–36) amide secretion in streptozotocin-induced diabetic rats

Lu¹,

Yu²,

Zhu³

et al. 2008

Journal of Endocrinology

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“…No GLP-1 receptor mRNA could be detected in brain, liver, thymus, muscle, intestine, and colon. The presence of the GLP-1 receptor has been reported in stomach, where the peptide inhibits acid secretion by parietal cells in in vivo experiments (33) but stimulates acid secretion on isolated parietal glands (34). Binding sites for GLP-1 have also been reported in lung membrane preparations (35) but the role of the hormone in lung physiology is not known.…”

Section: ---------------------------------------------38 Secr Luuaulymentioning

confidence: 99%

Expression cloning of the pancreatic beta cell receptor for the gluco-incretin hormone glucagon-like peptide 1.

Thorens

1992

Proc. Natl. Acad. Sci. U.S.A.

803

499

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Glucagon-like peptide 1 (GLP-1) is a hormone derived from the preproglucagon molecule and is secreted by intestinal L cells. It is the most potent stimulator of glucose-induced insulin secretion and also suppresses in vivo acid secretion by gastric glands. A cDNA for the GLP-1 receptor was isolated by transient expression ofa rat pancreatic islet cDNA library into COS cells; this was followed by binding of radiolabeled GLP-1 and screening by photographic emulsion autoradiography. The receptor transfected into COS cells binds GLP-1 with high affinity and is coupled to activation of adenylate cyclase. The receptor binds specifically GLP-1 and does not bind peptides ofrelated structure and similar function, such as glucagon, gastric inhibitory peptide, vasoactive intestinal peptide, or secretin. The receptor is 463 amino acids long and contains seven transmembrane domains. Sequence homology is found only with the receptors for secretin, calcitonin, and parathyroid hormone, which form a newly characterized family of G-coupled receptors.Glucose-induced insulin secretion is modulated by a number of hormones and neurotransmitters. In particular, two gut hormones, glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP), potentiate the effect of glucose on insulin secretion and are thus called gluco-incretins (1, 2). GLP-1 is a gluco-incretin in rat and in man (1-3). It is part of the preproglucagon molecule (4) that is proteolytically processed in intestinal L cells to GLP-1-(1-37) and GLP-1-(7-36) amide or GLP-1-(7-37) (5, 6). Only the truncated forms of GLP-1 are biologically active and both have identical effects on insulin secretion in ,. cells (7, 8). They are the most potent gluco-incretins so far described and are active at concentrations as low as 1-10 pM. The stimulatory effect of these gluco-incretin hormones requires the presence of glucose at or above the normal physiological concentration of about 5 mM and is mediated by activation of adenylate cyclase and a rise in the intracellular concentration of cAMP (9, 10). GLP-1 has also a stimulatory effect on insulin gene transcription (9). In rat, non-insulin-dependent diabetes mellitus (NIDDM) is associated with a reduced stimulatory effect of GLP-1 on glucose-induced insulin secretion (11). In man, in one study, GLP-1 levels were elevated in NIDDM patients in the basal state and after glucose ingestion; however, following a glucose load there was only a very small rise in plasma insulin concentration (12). This suggests that diabetic 3 cells, in addition to being glucose-unresponsive, may also have a decreased sensitivity to the incretin effect of GLP-1. However, a recent study (13) showed that GLP-1 infusion could ameliorate postprandial insulin secretion and glucose disposal in NIDDM patients, and this hormone, or derivatives thereof, has been proposed as a new therapeutic agent to stimulate insulin secretion by P cells of type II diabetic patients. Thus, as a further step in understanding the complex modulation ofinsulin secretion by gut...

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Section: Discussionmentioning

confidence: 99%

“…GLP-1 [7-36 amide] increases cyclic AMP and acid secre tion in isolated parietal cells of rats [20] and human gastric cancer cells [21]. In anesthe tized whole rats, GLP-1 [7-36 amide] was without effect on basal and pentagastrin-stim ulated gastric acid output [20]. The fact that GLP-1 [7-36 amide] stimulates gastric soma tostatin secretion [27], which under certain conditions may inhibit gastric acid secretion, does not explain this discrepancy because GIP also releases somatostatin from the iso lated perfused rat stomach [28], It may, how ever, be that direct (stimulatory) and soma tostatin-mediated indirect (inhibitory) effects of GLP-1 [7-36 amide] balance each other out under certain conditions.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 1992

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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.

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GLP-1-(7-36) amide, -(1-37), and -(1-36) amide: potent cAMP-dependent stimuli of rat parietal cell function

Cited by 20 publications

References 0 publications

Berberine promotes glucagon-like peptide-1 (7–36) amide secretion in streptozotocin-induced diabetic rats

Berberine promotes glucagon-like peptide-1 (7–36) amide secretion in streptozotocin-induced diabetic rats

Expression cloning of the pancreatic beta cell receptor for the gluco-incretin hormone glucagon-like peptide 1.

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

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