Failure of Endogenous Gastrin Release to Affect Serum Insulin

Budillon, G; Mazzacca, G; Squame, G

doi:10.1159/000197315

Cited by 3 publications

(3 citation statements)

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“…Basal gastric acid output (BAO) was measured on four 15-min aspirates collected before histamine stimulation. Maximal gastric acid output (MAO) was determined as previously described [5], Serum gastrin measurements were performed in triplicate by radioimmunoassay as previously reported (1). Antiserum was supplied by Wilson Laboratories, Chicago, III.…”

Section: Methodsmentioning

confidence: 99%

Serum Gastrin in Patients with Cirrhosis of the Liver

Mazzacca¹,

Budillon²,

Marco³

et al. 1974

Digestion

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Serum gastrin concentrations were examined following atropinization in 30 patients with liver cirrhosis and in 30 control subjects either basally or after oral glycine load. Basal gastrinaemia and post-glycine serum increases above basal levels were found to be significantly greater in the cirrhotic group (48.56 ± 9.97 and 72.85 ± 10.88 pg/ml, respectively) than in the control group (32.36 ± 6.67 and 53.43 ± 9.67 pg/ml, respectively) (ρ < 0.001). Furthermore, the post-glycine serum gastrin rise appeared to be more prolonged in the cirrhotic group than in the control subjects. The serum gastrin changes in cirrhotics did not appear to be caused by gastric hypoacidity. There was no correlation in cirrhotic patients between the magnitude of the post-glycine serum gastrin rise and the severity of liver insufficiency.

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Section: Methodsmentioning

confidence: 99%

Serum Gastrin in Patients with Cirrhosis of the Liver

Mazzacca¹,

Budillon²,

Marco³

et al. 1974

Digestion

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“…These results suggest that physiological concentrations of gastrin contribute little to the insulin response. Budillon et al [9], who studied gastrin and insulin release following oral and intraduodenal stimuli, reached similar conclusions. Rehfeld and Stadil [10] have shown that intravenous administration of gastrin will only stimulate insulin release when administered in doses which result in serum gastrin concentrations above the physiological range.…”

Section: Discussionmentioning

confidence: 66%

Gastrin and insulin release

1975

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Summary. Gastrin and insulin levels following protein ingestion were measured in control subjects, in patients with vagotomy and pyloroplasty and in patients with vagotomy, antrectomy and gastroenterostomy. Peak gastrin levels preceded peak insulin levels, but no relationship between gastrin output and insulin output was found. The insulin response in patients with impaired gastrin release was similar to that seen in patients with normal gastrin release. Insulin levels after oral glucose in patients with malignant Zollinger-Ellison syndrome were similar to those in patients after gastrectomy, in spite of marked differences in gastrin level. These studies do not suggest that gastrin stimulates insulin release.Key words: Gastrin, insulin, immunoassay, oral protein, oral glucose, antrectomy, Zollinger-Ellison syndrome.Oral administration of glucose causes a greater rise in plasma immunoreactive insulin (IRI) concentration than intravenous glucose [1], suggesting that intestinal factors augment the insulin response to the oral stimulus. In man, the intravenous administration of the antral hormone gastrin has been shown both to stimulate insulin release [2,3], and to be without effect [4]. The present investigation used radioimmunoassay techniques to study the effect of endogenous gastrin on insulin release in man. Material and MethodsEight control patients of normal weight and without clinical evidence of diabetes mellitus were studied. After an overnight fast they were given a standard protein meal of cooked minced meat (25 g protein in 200 ml). Peripheral venous samples for hormone assay were taken from a catheter placed in a forearm vein at 0, 15, 30, 45, 60, 90 and 120 min after protein ingestion. The plasma was separated and stored at --20~ until assayed. Estimates of the gastrin response were made by measurement of the area under the gastrin curve and above the projected basal [5]. The insulin response was assessed in a similar manner.Ten patients were studied following surgery for chronic duodenal ulceration. Seven, aged 46 + 3 (mean + SEM) years were studied following vagotomy and pyloroplasty and three years aged 42 + 7 (mean + SEM), were studied following vagotomy, antrectomy and gastroenterostomy. These patients were given the standard protein meal at least six weeks after surgery.

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“…5) Gastrin secretion in duodenal ulcer patients is also abnormally increased, at least during meals (35,36). Serum levels in these patients and those of food-stimulated normal subjects (37) are, however, placed so much to the left on the dose-response curve (4) that it is difficult to demarcate insulinogenic effects of endogenous gastrins in these conditions. 6) Patients with severe kidney damage are hypergastrinemic, but their general metabolic derangement, including abnormal levels of betacytotrophic hormones other than gastrin, makes them unfit for studies like the present.…”

Section: Discussionmentioning

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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Failure of Endogenous Gastrin Release to Affect Serum Insulin

Cited by 3 publications

References 7 publications

Serum Gastrin in Patients with Cirrhosis of the Liver

Serum Gastrin in Patients with Cirrhosis of the Liver

Gastrin and insulin release

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

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