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

Suspensions of viable cells were prepared from solid tumor of the Snell adrenocortical carcinoma 494 without the use of proteolytic enzymes. Cyclic AMP formation in these cells was stimulated by ACTH, LH, FSH and TSH but not by prostaglandins (E1, E2, F1alpha and F2alpha), insulin and secretin. Glucagon tested at a single dose level of 50 mug increased cyclic AMP to about 65% of the maximum amounts obtained with ACTH. When Ca++ was omitted from the incubation medium, the response to ACTH was considerably reduced while that to LH was essentially unchanged. Low concentrations of EGTA (0.3 MM) abolished the ACTH response almost completely but caused only a partial reduction in the response to LH; as much as 10 mM EGTA was required to obtain complete inhibition of the latter.
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PMID:Cyclic AMP response of isolated Snell adrenocortical carcinoma 494 cells to trophic hormones and other substances. 17 10

Cystic glucagonoma in contact with insulinoma was found in the pancreas of a 28-year-old female patient with characteristic hypoglycemic syndrome. Among six tumors in total detected in the tail of the resected pancreas, the largest solid tumor (2.5 cm in diameter) consisted mostly of insulin-containing cells with conspicuous amyloid deposition. Contiguous to this tumor, the second largest nodule, measuring 1.8 cm in diameter, showed cystic changes and consisted of glucagon-containing cells. High concentration of immunoreactive glucagon was demonstrated in the cystic fluid. In addition to the cystic changes of endocrine pancreatic tumors, simultaneous occurrence of glucagonoma in contact with insulinoma appears to be extremely rare and repeated episodes of hypoglycemia may contribute to its pathogenesis.
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PMID:Cystic pancreatic glucagonoma in contact with insulinoma found in a hypoglycemic patient. 143 39

We have found many compounds that amplify the action of glucocorticoid without themselves having any glucocorticoid-like action and have proposed the concept of 'Glucocorticoid Action Biomodulators'. These biomodulators consist of 'Glucorticoid Sensitivity Amplifiers', which greatly amplify the action of glucocorticoid at doses of glucocorticoid that alone have minimal effects, and 'Glucocorticoid Potency Amplifiers', which markedly enhance the effect of glucocorticoid at doses that have maximal effects. Potent activators of protein kinase C, such as 1,2-racemic dioctanoylglycerol, 12-o-tetradecanoyl-phorbol-13-acetate, and epidermal growth factor (EGF), markedly enhanced the induction of tyrosine aminotransferase and ornithine decarboxylase by dexamethasone in adrenalectomized rats in vivo and in primary cultures of adult rat hepatocytes in vitro. They amplified enzyme induction by even a large amount of dexamethasone that had a maximal effect, but had no effect in the absence of glucocorticoid. These modes of amplification show that these compounds are 'Glucocorticoid Potency Amplifiers'. They amplified not only enzyme induction in liver but also growth inhibition by glucocorticoid of solid tumor L5178Y lymphoblasts. They specifically amplified the actions of glucocorticoids and did not amplify the actions of other steroids, such as 17-beta estradiol, glucagon and insulin. The induction of tyrosine aminotransferase by glucocorticoid and its amplification by EGF were both inhibited by 1-(5-iso-quinoline-sulfonyl)-2-methylpiperazine, an inhibitor of protein kinase C, and not by N-[2-(methylamino)-ethyl]-5-isoquinoline-sulfonamide, an inhibitor of cyclic nucleotide dependent protein kinases, suggesting that the induction and the amplification are mediated by protein kinase C.
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PMID:Studies on biomodulators of glucocorticoid actions; the nature and the modes of actions of glucocorticoid potency amplifiers. 289 Feb 79

A 73-year-old woman was admitted to our department for treatment of diabetes (plasma glucose 289 mg/dl, HbA(1C) 7.1%, and glycated albumin 34.9%). She displayed the signs and symptoms of glucagonoma syndrome, including necrolytic migratory erythema (NME), low aminoacidemia, and a marked increase of the serum glucagon level (4,940 pg/ ml). Thus, we suspected a glucagonoma causing secondary diabetes. However, we could not detect any mass in the pancreas or the gastrointestinal tract, and only found a liver lesion resembling a hemangioma. Her NME improved markedly after intravenous infusion of amino acids, and her plasma glucose was controlled reasonably well by intensive insulin therapy. However, her general condition deteriorated and she died on day 57 after hospitalization. At autopsy, the only tumor detected was the liver mass. This was a large solid tumor (8 x 6 x 5 cm) with a pattern of white and dark brown stripes located in the left lobe, while two white nodules were also found in the right lobe. Based on the histopathological and immunohistochemical findings, the liver lesion was shown to be a malignant glucagonoma with intrahepatic metastases. Since primary malignant hepatic glucagonoma has not been reported before, we present this extremely rare case of primary malignant glucagonoma of the liver.
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PMID:Primary malignant hepatic glucagonoma: an autopsy case. 1936 16