Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin hypoglycaemia causes a rise in plasma vasopressin concentrations in man and the rat, and vasopressin stimulates glucagon secretion and increases hepatic glucose output in man. Vasopressin has also been suggested to have an important synergistic role with corticotrophin releasing factor in the release of adrenocorticotrophin hormone, and a counter-regulatory role for the hormone has been proposed. As diminished anterior pituitary hormone responses to hypoglycaemia have been reported in diabetes mellitus, we studied the plasma vasopressin responses to insulin-induced hypoglycaemia in 10 patients with established Type 1 diabetes and 10 matched control subjects. Blood glucose fell from 4.5 +/- 0.3 to 1.6 +/- 0.1 mmol l-1 (p less than 0.001) in the diabetic group and from 4.6 +/- 0.2 to 1.5 +/- 0.2 mmol l-1 (p less than 0.001) in control subjects, with delayed blood glucose recovery in the diabetic patients. Plasma vasopressin rose in the diabetic patients from 0.9 +/- 0.2 to 6.9 +/- 2.8 pmol l-1 (p less than 0.001), a significantly greater rise (p less than 0.05) than in the control subjects, 0.8 +/- 0.1 to 2.4 +/- 1.0 pmol l-1 (p less than 0.001). Plasma osmolalities remained unchanged and haemodynamic changes were similar in both groups. There is an exaggerated rise in plasma vasopressin concentrations in diabetic patients in response to insulin-induced hypoglycaemia. The putative mechanisms and potential significance of the exaggerated rise are discussed.
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PMID:Vasopressin secretion during insulin-induced hypoglycaemia: exaggerated responses in people with type 1 diabetes. 252 60

Previous studies demonstrated that insulin-induced hypoglycemia enhances glicentin secretion in piglets and prompted us to investigate the response of glucagon-like immunoreactivity (GLI) to hypoglycemia in dogs. Insulin hypoglycemia did not induce any rise of plasma total immunoreactive glucagon (IRG) measured by nonspecific antiserum to glucagon in normal or pancreatectomized dogs under anesthesia. In contrast, insulin-induced hypoglycemia clearly increased plasma total IRG in both normal and pancreatectomized dogs in a conscious state. Administration of acetylcholine resulted in an elevation of plasma total IRG, whereas epinephrine induced a slight increase in plasma total IRG. The infusion of alpha- or beta-adrenergic blockers did not affect the response of plasma total IRG to hypoglycemia, whereas atropine completely blunted the increase in plasma total IRG during insulin hypoglycemia. Similarly atropine abolished the rise of plasma total IRG during intravenous administration of 2-deoxy-D-glucose. It is concluded that hypoglycemia clearly enhances the secretion of GLI from the gut in dogs and that GLI secretion during hypoglycemia is modulated, at least in part, by the autonomic nervous system.
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PMID:Response of gut glucagon-like immunoreactivity to hypoglycemia in dogs. 264 47

In 142 test persons the insulin hypoglycaemia test as well as the glucagon propranolol test were performed under the interrogation of a hyposomatotropism. The combination of these tests proved as suitable for the answers to this inquiry. The insulin hypoglycaemia test led in 29%, the propranolol glucagon test only in 6% to the false indication of a hyposomatotropism. Thus the propranolol glucagon test has the higher diagnostic certainty. Insulin hypoglycaemia test and propranolol glucagon test seem to have a different effect.
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PMID:[The value of growth hormone stimulation tests]. 702 33