Stimulation of Insulin Secretion by the C-Terminal Tetrapeptide Amide of Gastrin

Kaneto, Akio; Tasaka, Yoshimasa; Kosaka, Kinori; Nakao, Kiku

doi:10.1210/endo-84-5-1098

Cited by 22 publications

(12 citation statements)

References 2 publications

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“…It was previously reported (8) that 33-amino acid pancreozymin-cholecystokinin increases somatostatin release. Thus, the D cell appears to be a possible target of at least four of the alimentary hormones that influence the B and A cells (14)(15)(16)(17)(18)(19)(20)(21). With each hormone the pattern of the somatostatin response was remarkably similar to that of insulin.…”

Section: Resultsmentioning

confidence: 98%

The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of cholecystokinin upon immunoreactive somatostatin release by the perfused canine pancreas.

Ipp¹,

Dobbs²,

Harris³

et al. 1977

J. Clin. Invest.

114

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A B S T R A C T The effects ofgastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of pancreozymin-cholecystokinin on immunoreactive somatostatin release were studied in the isolated perfused dog pancreas. Gastrin at a concentration of 65 ng/ml and the octapeptide of pancreozymin-cholecystokinin at a c.oncentration of 25 ng/ml produced a prompt, but transient statistically significant, twofold rise in mean somatostatin concentration. Secretin at a concentration of 0.3 U/ml and gastric inhibitory polypeptide concentration of 58 ng/ml produced a prompt two-to threefold rise in mean somatostatin release, which persisted throughout the perfusion period. With all four polypeptides the pattern of the somatostatin response resembled that of insulin. It appears that pancreatic somatostatin release is stimulated by gastrointestinal hormones that influence the secretion of insulin and glucagon.

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Section: Resultsmentioning

confidence: 98%

The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of cholecystokinin upon immunoreactive somatostatin release by the perfused canine pancreas.

Ipp¹,

Dobbs²,

Harris³

et al. 1977

J. Clin. Invest.

114

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show abstract

“…Mean-gastrin concentration ± 1 SD was 84.4±3.9 pmol per liter and 13.4±4.8 pmol per liter respectively. Between-assay reproducibility was tested during 21 assays covering a period of 4 mo; for three sera the mean and standard deviations were 24.0±0.8, 8.1+1.8, and 43.4±3.0 pmol per liter. The relative accuracy was estimated by comparison of reference concentrations with those reported by other groups.…”

Section: Laboratory Methodsmentioning

confidence: 99%

The Effect of Gastrin on Basal- and Glucose-Stimulated Insulin Secretion in Man

Rehfeld¹,

Stadil²

1973

J. Clin. Invest.

157

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A B S T R A C T The effect of gastrin on basal-and glucose-stimulated insulin secretion was studied in 32 normal, young subjects. The concentration of gastrin and insulin in serum was measured radioimmunochemically.Maximal physiologic limit for the concentration of gastrin in serum was of the order of 160 pmol per liter as observed during a protein-rich meal. Oral ingestion of 50 g glucose produced a small gastrin response from 28±3 to 39+5 pmol per liter (mean +SEM, P < 0.01).Intravenous injection or prolonged infusion of gastrin increased the concentration of insulin in peripheral venous blood to a maximum within 2 min followed by a decline to basal levels after a further 10 min. The The results indicate that gastrin can stimulate a rapid and short-lived release of insulin. In physiologic concentrations gastrin potentiates the glucose-stimulated insulin secretion and is without effect on basal insulin secretion. A small release of gastrin during oral glucose ingestion may to a limited extent contribute to the nonglycemic insulin secretion. During protein ingestion, gastrin probably stimulates insulin secretion significantly.This work was presented in part at the International Symposium on "The impact of insulin on metabolic pathways," 26 October 1971, Jerusalem, Israel.

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“…In regard to the insulin-releasing effects shown by exogenously ad ministered gastrin, as reported by some authors [3], the discrepancy is probably explained by the fact that the injected hormone was administered in pharmacological amounts not usually attained under physiological conditions.…”

Section: Discussionmentioning

confidence: 92%

“…Indeed, several reports furnish evidence that gastrin [3] as well as other gastrointestinal hormones [1,8,9] are capable of releasing insulin in vivo and in vitro.…”

mentioning

confidence: 99%

Failure of Endogenous Gastrin Release to Affect Serum Insulin

1973

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The effect of endogenously stimulated gastrin on serum insulin level was investigated in 7 normal subjects. Glycine by mouth was chosen as gastrin releaser. The glycine drink caused a significant rise of serum gastrin and insulin levels either in the fasting state or during glucose stimulation. However, serum insulin response of same magnitude occurred when stimulation of gastrin secretion was prevented to occur by infusing glycine into the duodenum. The results suggest that post-glycine rise in serum insulin was not mediated by endogenous gastrin release.

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Stimulation of Insulin Secretion by the C-Terminal Tetrapeptide Amide of Gastrin

Cited by 22 publications

References 2 publications

The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of cholecystokinin upon immunoreactive somatostatin release by the perfused canine pancreas.

The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of cholecystokinin upon immunoreactive somatostatin release by the perfused canine pancreas.

The Effect of Gastrin on Basal- and Glucose-Stimulated Insulin Secretion in Man

Failure of Endogenous Gastrin Release to Affect Serum Insulin

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