Effect of the C-Terminal Tetrapeptide Amide of Gastrin on Insulin Secretion in Man

Ohgawara, Hisako; Mizuno, Yoshiatsu; Tasaka, Yoshimasa; Kosaka, Kinori

doi:10.1210/jcem-29-9-1261

Cited by 20 publications

(11 citation statements)

References 1 publication

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“…4) response to oral glucose is particularly pronounced in those duodenal ulcer patients who exhibit high levels of basal acid secretion. The finding of hyperglycaemia at a time when plasma insulin levels are raised, suggesting a degree of resistance to the peripheral actions of insulin, is in keeping with the concept of an increased release of small-bowelhormones, since some of these hormones are known to exert, either directly or indirectly, a hyperglycaemic effect (Unger and Eisentraut, 1964;Unger et al, 1967;Ohgawara et al, 1969).…”

Section: Discussionsupporting

confidence: 55%

Glucose Tolerance and Insulin Secretion in Patients with Chronic Duodenal Ulcer

Humphrey¹,

Dykes²,

Johnston³

1972

BMJ

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Section: Discussionsupporting

confidence: 55%

Glucose Tolerance and Insulin Secretion in Patients with Chronic Duodenal Ulcer

Humphrey¹,

Dykes²,

Johnston³

1972

BMJ

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“…Concerning the action of gastrin on insulin secretion, several investigators (Unger et al, 1967;Unger and Eisentraut, 1969;Dupre et al, 1969;Kaneto et al, 1969;Ohgawara et al, 1969;Rehfeld and Stadil, 1973) have reported that gastrin stimulates insulin release, and others (Jarett et al, 1967;Lazarus et al, 1968;Buchanan et al, 1969;Pointner et al, 1974;Hayes et al, 1975b) have reported that gastrin has no effect on insulin release. This conflicting result may be in part due to the use of pharmacological doses of crude preparations of fragment of gastrin.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of somatostatin on insulin and gastrin secretion in dogs.

Ishida

1977

Endocrinol Japon

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“…Exogenous gastrin in form of the heptadecapeptide amide (gastrin-17)1 and its C-terminal tetrapeptide amide can stimulate insulin release in man (1)(2)(3). But dose-response studies with exogenous gastrin-17 correlated to endogenous gastrin concentrations in serum during meals point to a limited role of gastrin in the regulation of insulin secretion in normal human subjects (4).…”

Section: Introductionmentioning

confidence: 99%

Disturbed islet-cell function related to endogenous gastrin release. Studies on insulin secretion and glucose tolerance in pernicious anemia.

Rehfeld¹

1976

J. Clin. Invest.

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A B S T R A C T The insulin and gastrin response to oral glucose, intravenous glucose, or a protein-rich meal were measured in 44 nondiabetic patients with pernicious anemia (PA) and in 44 control subjects. 36 of the PApatients had hypergastrinemia, while serum gastrin concentrations in the remaining eight patients were below normal. Three hypergastrinemic PA-patients were in addition studied during an oral glucose loading with synchronous intravenous infusion of gastrin-17.During both oral and intravenous glucose tests blood glucose concentrations were similar in patients and in controls. After ingestion of protein blood glucose concentrations in PA-patients with hypergastrinemia were above those of the controls (P <0.05). Parenteral infusion of gastrin-17 during oral glucose loading also increased blood glucose concentrations above the levels observed after glucose alone. In PA-patients with hypergastrinemia the insulin response was augmented in all tests. In patients with hypogastrinemia serum insulin concentrations were lower than normal in the fasting state and during stimulation with glucose intravenously (P < 0.01). In hypergastrinemic patients serum gastrin concentrations decreased after oral as well as intravenous glucose administration. The decrease was larger during the oral test. In hypogastrinemia oral glucose induced, as in controls, a small initial rise followed by a slow fall in serum gastrin concentrations. No variations were seen in these patients during the intravenous glucose infusion. Gel filtration of serum from hypergastrinemic patients disclosed a decrease in the concentrations of all Dr. Rehfeld's present address is Institute of Medical Biochemistry, University of Aarhus, DK-8000 Aarhus C, Denmark.Received for publication 1 December 1975 and in rezHsed form 16 February 1976. four main components of gastrin during the glucose loadings.Taken together with earlier studies on the effect of exogenous gastrin the results suggest that endogenous hypergastrinemia induces hyperglycemia and potentiates insulin secretion. In contrast hypogastrinemia is associated with hypoinsulinism.

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Effect of the C-Terminal Tetrapeptide Amide of Gastrin on Insulin Secretion in Man

Cited by 20 publications

References 1 publication

Glucose Tolerance and Insulin Secretion in Patients with Chronic Duodenal Ulcer

Glucose Tolerance and Insulin Secretion in Patients with Chronic Duodenal Ulcer

Inhibitory effect of somatostatin on insulin and gastrin secretion in dogs.

Disturbed islet-cell function related to endogenous gastrin release. Studies on insulin secretion and glucose tolerance in pernicious anemia.

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