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)

24 diabetics, (9 thin diabetics, 14 cases of maturity onset diabetes, 6 intermediate forms and one case of partial pancreatectomy) received 7.5 to 20 mg of bromocriptine (CB 154) per 24 hours. A definite improvement in glucose metabolism was noted in 6 cases, a definite aggravation in 4 cases; 14 results were not significant (p-0.05). The efficacy of CB 154 did not depend on the clinical type nor on the patient's age. It appeared related to duration of the diabetes (2 years and 3 months in improved patients, 11 years in aggravated patients) and perhaps the degree of retinopathy (more frequent and severe in aggravated patients). The improvement seems to be linked to the existence in certain diabetics of a paradoxical regulation of STH secretion as in acromegaly. The possibility of a peripheral effect of bromocriptine on insulin and glucagon is discussed. The CB 154 test (estimations of STH after a single dose of 2.5 mg) permits one to foresee the efficacy of the drug and perhaps the risk of diabetic retinopathy.
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PMID:[Action of bromocriptine on glucose metabolism in diabetics]. 20 Oct 30

The glucagonoma syndrome occurs in some but not all patients with a benign or malignant islet cell tumor and hyperglucagonemia. Manifestations may include anemia, diabetes mellitus, pruritic skin rash, glossitis, stomatitis, weight loss, diarrhea, flexible fingernails, venous thromboses, low plasma amino acid levels, and coarse folds of the jejunum and ileum. Most patients are postmenopausal women, but men and women ages 40 to 65 have been affected. The course is variable depending upon the nature of the underlying tumor. Twenty-two cases of probable glucagonoma syndrome have been reported; twelve documented with glucagon levels. The hyperglucagonemia results from elevation of the proglucagon and true glucagon immunoreactive fractions of pancreatic glucagon. Management of the rash can be accomplished rarely with topical or systemic antibiotics or corticosteroids. If the tumor is resectable, surgery reverses the syndrome. Patients with metastatic disease have responded to streptozotocin and DTIC.
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PMID:The glucagonoma syndrome and its management. 20 9

Hyperglycemia, glucose intolerance, hyperinsulinemia and resistance to exogenous insulin were found in a 10-year-old Japanese boy diagnosed as having congenital generalized lipodystrophy. Studies on insulin receptors of circulating mononuclear leucocytes indicated that insulin-resistant diabetes combined with congenital generalized lipodystrophy may be due to disturbance of insulin binding to membrane receptors. No insulin-binding antibody or antibody that impairs insulin-receptor binding was found. Plasma glucagon showed an exaggerated response to L-arginine before treatment. After treatment with a controlled diet and an oral sulfonylurea (500 mg/day) for 4 weeks, there was improvement in the plasma glucagon response to L-arginine. Improvement in the hyperglycemia, hyperinsulinemia and acanthosis nigricans was also observed. On the other hand, on completion of a 7-day high-fat diet, a marked increase in serum free fatty acids, triglycerides and beta-lipoproteins was observed. The total plasma post-heparin lipolytic activity during the high fat diet was within the normal range. However, the level of protamine-inactivated activity was 3 times that of the control.
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PMID:Congenital generalized lipodystrophy with insulin-resistant diabetes. 20 64

The regional concentrations and in-vitro secretions of canine pancreatic polypeptide (cPP), insulin, and glucagon were studied. CPP is found predominantly in the uncinate process of the dog pancreas, whereas insulin and, more markedly, glucagon predominate in the body and tail of the pancreas. In-vitro secretion studies of pancreatic pieces indicate that dibutyryl cyclic AMP (dcAMP) alone can stimulate cPP release whereas glucose and arginine alone have no effect. Arginine, but not glucose, potentiates this stimulant effect of dcAMP. These studies suggest that the cAMP generating system may play a role in regulation of cPP secretion.
Diabetes 1978 Feb
PMID:Regional pancreatic concentration and in-vitro secretion of canine pancreatic polypeptide, insulin, and glucagon. 20 6

Ketotic, insulin-requiring diabetes mellitus and a severe peripheral neuropathy developed in a previously healthy 25-year-old man several days after he attempted suicide with rat poison containing N-3-pyridylmethyl N'-p-nitrophenyl urea. Study of islet-cell function ten months after ingestion showed a reduced disappearance rate of intravenous glucose and depressed C-peptide response to intravenous glucose when compared with a normal control but no impairment of glucagon release after intravenous arginine stimulation. Nerve conduction studies demonstrated severe sensory and mild motor neuropathy. Quadriceps capillary basement membrane thickness was in the diabetic range. Because at least 15 similar occurrences have been reported to the manufacturer, this agent appears to be diabetogenic in man, probably causing beta-cell destruction. Niacinamide, which can prevent glucose intolerance in both streptozocin- and alloxan-treated animals and prevents death in rats given this rodenticide, may be a useful antidote.
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PMID:Diabetes mellitus following rodenticide ingestion in man. 20 29

The glucagonoma syndrome is characterized by necrolytic migratory erythema, glossitis, ungual dystrophy, diabetes mellitus, anemia, weight loss, elevated plasma glucagon levels and an alpha-cell glucagon-secreting neoplasm of the pancreas. We are reporting a case of this syndrome in a middle-aged woman, in whom the first complaints and signs were cutaneous. The recognition of the distinctive skin manifestations of the syndrome led to early diagnosis and treatment of the underlying malignant pancreatic tumor.
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PMID:The glucagonoma syndrome. 20 68

We have previously shown that adipocytes from adult (between four and five months old) rats have reduced glucagon binding and glucagon-stimulated lipolytic activity when compared with cells from young (1.5 months old) animals. In the present study we measured specific [125I] glucagon binding by purified liver plasma membranes isolated from young and adult rats. When expressed on the basis of membrane protein content, 5'-nucleotidse activity, or specific [125I] insulin binding, the extend of [125I] glucagon binding by liver membranes was not influenced by aging. Furthermore, the degree of [125I] glucagon degradation was the same in both membrane preparations. These data describe a unique condition in which glucagon binding and hormone sensitivity diminish in one tissue but remain unaltered in another.
Diabetes 1978 May
PMID:[125I] Glucagon binding by liver membranes from young and adult rats. 20 81

Venous blood returning from the splanchnic viscera has liver-supporting (hepatotrophic) qualities not found to the same degree in other kinds of arterial or venous blood. The effects of portal blood have been noted in animals with two livers (or a differential portal blood supply to different regions of one liver) to include hypertrophy, glycogen storage, hyperplasia, capacity for regeneration, increase of several synthetic functions, and maintenance of normal structure. The main splanchnic venous hepatotrophic factors are endogenous hormones of which the single most important is insulin. Thus, the foregoing portal hepatotrophic effects are largely eliminated with the diabetes produced by alloxan or total pancreatectomy. The injury of portacaval shunt is caused by the diversion of the hormones around the liver. Accordingly, the atrophy, injury to the organelles, and loss of the capacity for cell renewal is minimized if insulin is infused into the portally deprived liver. In these and other experiments, exogenous glucagon alone or the addition of glucagon to insulin has had no effect, but this may be because of the masking presence of gut glucagon and other hormonal or non-hormonal substances in our models. At present, the effects on the liver of exogenous insulin, glucagon, epidermal growth factor, and numerous other hormones are being determined by their intraportal infusion into eviscerated dogs in which other endogenous splanchnic factors have been eliminated.
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PMID:A hundred years of the hepatotrophic controversy. 20 94

The effects of endogenous and exogenous hyperglucagonemia on the specific binding of glucagon to hepatocyte receptors was studied, as was the response of cAMP to glucagon. In streptozotocin diabetic rats, blood glucose and plasma glucagon increased and plasma insulin decreased as compared with controls. Insulin treatment in diabetic rats restored blood glucose and plasma glucagon toward normal and elevated plasma insulin. Specific binding of (125)I-glucagon to isolated hepatocytes (10(6) cells) decreased in diabetic rats (8.17+/-0.38%) compared to controls (14.05+/-0.87%) and was restored by insulin treatment (12.25+/-0.93%). Specific binding of (125)I-insulin in controls was 7.30+/-10.16%; it increased in diabetic rats to 12.50+/-0.86%, and decreased in diabetic rats after insulin treatment (9.08+/-0.87%). Scatchard analysis and the competition plots of the data indicate that decreased glucagon binding and increased insulin binding in diabetes were due to change in the number of receptors rather than a change in their affinity. Hepatocyte cAMP response to glucagon (0.25-5.0 ng/ml) was almost abolished in diabetic rats and was restored with insulin treatment. Specific glucagon binding by hepatocytes from chronically hyperglucagonemic (glucagon injected) rats was decreased (P < 0.005) to 8.76+/-0.61% compared with controls (13.20+/-0.74%) and acutely hyperglucagonemic animals (13.53+/-1.33%). The decreased binding was associated with a 70% decrease in hepatocyte cAMP response to glucagon compared with a normal response in acutely hyperglucagonemic rats.These data appear to support the concept of receptor regulation by ambient hormone level. In both endogenous and exogenous hyperglucagonemia, however, there was a disproportionately large decrease in cAMP response to glucagon compared to the decrease in glucagon binding.
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PMID:Decreased glucagon receptors in diabetic rat hepatocytes. Evidence for regulation of glucagon receptors by hyperglucagonemia. 20 37

Thus far, somatostatin has been used primarily as a research tool to investigate pancreatic alpha- and beta- cell function. On the basis of its ability to inhibit insulin and glucagon secretion, several therapeutic applications have been suggested: e.g., as an adjunct in the treatment of diabetes mellitus, or as a palliative agent in inoperable islet tumors. Current experiments are underway to develop more specific analogs with longer durations of action to permit clinical evaluation of these potential applications. The presence of somatostatin within the pancreatic D cells raises the possibility that it may function as a local regulator of insulin and glucagon release. Clearly, further work is needed to delineate the factors governing the secretion of somatostatin and its mode of action. Such studies may uncover a new class of syndromes resulting from D-cell dysfunction.
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PMID:Somatostatin and the endocrine pancreas. 21 Oct 5


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