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)

Fasting hypoglycemia occurred in a patient with a histologically benign mesothelioma; the serum insulin was low (2-4 muU./ml.), as was the glucose utilization rate. Splanchnic glucose output was markedly decreased on direct measurement (21 mg./min.; normal: 108-180 mg./min.). Splanchnic uptake of gluconeogenic substrates plasma glucagon was low normal during hypoglycemia and responded poorly to oral and intravenous alanine. The nonsuppressible insulin-like (NSILA-s) and somatomedin-like activities of the serum were not elevated, and the tumor did not release insulin-like activity on incubation nor did it contain somatostatin. The marked decrease in splanchnic glucose output was the principal cause of hypoglycemia, was associated with an apparent decrease in glycogenolysis, and was at least partly due to deficient glucagon secretion. The relationship of the tumor to these defects is unclear. The tumor may have secreted an unknown insulin-like material affecting primarily the liver and/or pancreatic alpha cell. The approach used here may serve as a paradigm for the analysis of hypoglycemia not caused by excessive insulin.
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PMID:Tumor hypoglycemia: deficient splanchnic glucose output and deficient glucagon secretion. 125 10

A patient with biopsy-proved biliary cirrhosis and previous gastrojejunostomy and portacaval anastomosis experienced episodes of severe hypoglycemia. She was found to have hyperinsulinemia and hyperglucagonemia. An oral glucose tolerance test showed postgastrectomy hypoglycemia. Results of the intravenous tolbutamide test were diagnostic for insulinoma, but results of the intravenous glucagon test and prolonged fast (96 hours) were not. Failure, on two occasions, to suppress C-peptide normally during insulin-induced hypoglycemia led to a diagnosis of pancreatogenous hyperinsulinemia. The pancreas showed a 10-fold increase in islet volume, with intensely positive staining with anti-insulin and anti-glucagon antiserums in addition to anti-somatostatin and anti-pancreatic polypeptide antiserums. Incidental findings at pancreatic exploration were a mesothelioma, which did not stain with anti-insulin antiserum, and, at autopsy one year later, a hepatoma.
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PMID:Diagnosis of pancreatic islet hyperplasia causing hypoglycemia in a patient with portacaval anastomosis. 699 72

We treated four patients who had hypoglycemia and nonpancreatic tumors. Two had pleural mesothelioma, one had primary fibrosarcoma of the liver, and one had pheochromocytoma metastatic to the liver. We propose four mechanisms for this syndrome: (1) insulin or insulin-like activity produced by the tumor, (2) decreased gluconeogenesis, (3) disruption of glucagon metabolism, and (4) increased utilization of glucose by the tumor. The local effects of the tumor in hepatic parenchyma may also play an important role. The important diagnostic tests are an insulin-glucose ratio, to rule out insulinoma, and fasting glucose levels. An assay of nonsuppressible insulin-like activity can be performed and is of investigative interest, but does not aid in individual patient therapy. Treatment consists of control of the tumor.
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PMID:Causes and evaluation of tumor-induced hypoglycemia. 709 41

Hypoglycemia is a common emergency, and is usually due to insulin therapy or oral hypoglycemic treatment in diabetic patients. In some cases, hypoglycemia can be a paraneoplastic sign. We report the case of a 61-year-old woman with a malignant peritoneal mesothelioma, who was admitted to hospital because of diminished consciousness. The final diagnosis was paraneoplastic hypoglycemia with a positive response to glucagon. The patient was finally discharged with glucagon perfusion.
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PMID:[Glucagon perfusion in paraneoplastic hypoglycemia]. 1962 29