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)

17 oral glucose tolerance tests with simultaneous estimation of plasma insulin, were carried out in 15 patients with chronic pancreatitis of which 7 were of calcific type. Among these patients, 10 had obvious diabetes and 3 chemical diabetes. The disorders of glucose regulation were more common in the calcific form of the disease. Serum insulin was then lower and not stimulant. The curves of plasma insulin obtained in non-calcific pancreatitis were variable. In hyperinsulinism, the oral glucose tolerance test showed flat or normal curves. In hypoinsulinism, the glucose tolerance tests were either normal or strongly pathological. This insulinism, as shown by this study of chronic pancreatitis, seems to be linked to an imbalance in the cell distribution of the islets of Langerhans. The role of glucagon appears preponderant.
Sem Hop 1976 Dec
PMID:[Study of insulin secretion in chronic pancreatitis]. 18 95

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.
Sem Hop
PMID:[Action of bromocriptine on glucose metabolism in diabetics]. 20 Oct 30

Acute poisoning with beta adrenergic inhibitors is rare although such drugs are widely prescribed. Between 1966 and 1980, 40 cases were recorded at the Fernand-Widal Toxicology Center. 40% of patients were asymptomatic and 25% had sinus bradycardia. 35% of patients had specific toxic signs, either atrioventricular block (20%) or hemodynamic disorders (15%); the latter were seen only when associated heart disease was present or when another cardiotropic agent had been absorbed. No deaths were recorded. This favorable prognosis may result from the self-limited nature of poisoning with beta blocking agents, myocardial function being similar to that which follows denervation. In severe cases, management includes pacing and glucagon.
Sem Hop 1982 Apr 29
PMID:[Beta adrenergic receptor blockade : a self-limited phenomenon explaining the benignancy of acute poisoning with beta adrenergic inhibitors. Report of a series of 40 patients seen at the Fernand-Widal Toxicology Center, with a 0% mortality rate (author's transl)]. 612 35

Polypeptides are endogenous agents, involved in the regulation of many physiologic functions and the pathogenesis of several diseases. Polypeptide antagonists form a group of new chemical entities which may provide valid therapeutic agents. Some polypeptides (angiotensin, kinins) are released through the action of proteolytic enzymes (renin, kallikreins) and act as hormones or autacoids; others (substance P, neurotensin) are synthetized by nervous cells to serve as neurotransmitters or neuromodulators. The main homeostatic role of the renin-angiotensin system is to uphold high systemic arterial blood pressure. Overproduction of renin and insufficient checking of renin secretion are among the most common causes of arterial hypertension. Several forms of arterial hypertension (neurovascular, idiopathic) benefit from a reduction in renin-angiotensin system activity. This is achieved either through decreasing renin secretion, by inhibiting conversion of angiotensin I into angiotensin II, or through blocking the peripheral actions (at the receptor sites) of angiotensin II. Renin secretion is very significantly reduced by beta-blocking agents (propranolol); conversion of angiotensin I into angiotensin II is inhibited by teprotide, captopril and their derivatives; peripheral actions of angiotensin II are blocked by saralasin. Bradykinin and related agents produce vasodilation, increase vascular permeability and stimulate pain fibers. Kinins thus reproduce the cardinal features of inflammation and are held to be mediators of the inflammatory reaction. The substance P neuropeptide is found in the brain and bowel; it may act as a transmitter of the sensation of pain at the spinal cord and central nervous system sites. Among other effects outside of the brain, substance P is a potent vasodilator and inhibits renin secretion. Neurotensin is a neuropeptide which produces hypothermia, muscular relaxation and analgesia. Outside of the brain, this peptide is involved in the regulation of gastric secretion, intestinal motility and insulin and glucagon secretion. The vasoactive intestinal peptide, found in certain cholinergic nerve endings, is a large peptide which inhibits gastric secretion, intestinal motility and vascular tone.
Sem Hop 1984 Mar 29
PMID:[Polypeptides and antagonists]. 620 6

The mouse homeodomain protein insulin promoter factor-1 (IPF-1) and the rat homologue somatostatin transactivating factor-1 (STF-1) are involved in early pancreatic development and have been implicated in the cell-specific regulation of insulin- and somatostatin-gene expression in mature islet beta- and delta-cells. The cell specificity of IPF-1/STF-1 expression in mature islets is, however, still unclear. Using antisera against recombinant IPF-1 and STF-1 in combination with antisera against islet hormones we find that all beta-cells in monolayers of newborn rat islet cells express STF-1, as do a fraction of the delta-cells. In adult rat and mouse pancreas we find a similar distribution. IPF-1/STF-1 expression was not detected in glucagon-producing alpha-cells. In islet cell tumour models we found that a glucagon/islet amyloid polypeptide (IAPP)-producing pluripotent rat islet cell line (NHI-6F-GLU) expresses STF-1 in all cells prior to insulin gene activation induced by in vivo culture. In contrast, a mouse alpha-cell line (alpha TC1) exclusively expressed IPF-1 in a small subset of insulin-producing cells while an insulin-negative subclone (alpha TC1.9) was negative for IPF-1. In transfection experiments using alpha TC1.9 cells STF-1 activated a rat insulin 1 reporter gene dependent not only on both STF-1-binding sites, but also on the E1-binding site for the helix-loop-helix factor IEF-1. However, the endogenous mouse insulin genes remained inactive in these cells. These results suggest that the insulin promoter acquires its very high, yet cell-specific, activity at least partly through the action of IPF-1/STF-1. This action is dependent on helix-loop-helix factors bound to the E1 element.
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PMID:The homeodomain protein IPF-1/STF-1 is expressed in a subset of islet cells and promotes rat insulin 1 gene expression dependent on an intact E1 helix-loop-helix factor binding site. 757 38