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)

The influence of prostaglandin E1 and prostaglandin F2alpha on circulating concentrations of insulin and glucagon during the intravenous glucose tolerance test has been studied in normal man. Insulin responses to glucose during PGE1 infusion (0.2 microgram/Kg/min) were significantly lower than in control infusions (p less than 0.001 at 2, 5, 10 and 15 min). Moreover, PGE1 caused a clear elevation of basal glucagon (p less than 0.02). PGF2alpha, at the two doses used (0.2 and 0.5 microgram/Kg/min), had no effect on basal glucose, insulin and glucagon levels, nor upon glucose-induced insulin secretion. Neither prostaglandin affected the glucose-induced inhibition of pancreatic alpha-cells. There is thus some evidence that PGs of E series may play some role in modulating the secretion of human pancreatic beta-cells.
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PMID:Effects of prostaglandin E1 and prostaglandin F2alpha on insulin and glucagon plasma levels during the intravenous glucose tolerance test in man. 71 Jun 79

1. The effects of glucagon on the secretion of pancreatic juice were investigated using blood-perfused canine pancreas preparations. 2. Intravenous administration of glucagon (3-30 mug/kg) to the donor dog elicited a dose-dependent increase in pancreatic secretion. Intra-arterial administration of glucagon (10-100 mug) into the perfused pancreas also elicited increased secretion. 3. There were slight increases in amylase concentration of the pancreatic juice with the largest doses of glucagon given by either route. 4. Glucagon-induced secretion was not modified by treatment with phentolamine, propranolol, atropine, guanethidine, tetradotoxin, haloperidol, prostaglandin F2alpha or calcitonin. 5. The results suggest that glucagon acts directly on the exocrine cells of the canine pancreas.
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PMID:Effects of glucagon on pancreatic secretion in the dog. 97 53

Arachidonic acid metabolites are involved in a wide spectrum of hepatobiliary physiologic functions and disease. Prostanoids alter hepatic bile flow. Prostaglandins with a C9 ketooxygen stimulate a bicarbonate-rich choleresis and those with a C9 hydroxyloxygen produce a chloride-rich choleresis. Prostaglandin F2 alpha stimulates the release of the potent choleretic glucagon and the stimulatory effect of prostaglandin F2 alpha on bile flow is inhibited by cyclooxygenase inhibitors, suggesting that prostaglandins play a role in the release of choleretic hormones as well as in their action. Prostanoids are involved in gallbladder contraction and water absorption. Prostaglandins produce gallbladder contraction in various species and cause gallbladder relaxation in other species. Prostaglandins also may be mediators of cholecystokinetic hormone action; however, cyclooxygenase inhibitors do not inhibit the effect of cholecystokinetic hormones in all species. Prostanoids alter the normal process of water absorption by gallbladder mucosa and induce net water secretion. The inflamed gallbladder secretes rather than absorbs fluid. The demonstration that prostaglandin E2 inhibits gallbladder fluid absorption has led to subsequent studies that demonstrated that the secretion of fluid into the inflamed gallbladder lumen may be mediated by prostanoids. In cholecystitis, the prostanoids may mediate the distention produced by mucosal fluid secretion and the contraction of the diseased gallbladder. The inflammatory changes produced in various experimental models of cholecystitis can be prevented by cyclooxygenase inhibitors. Cyclooxygenase inhibitors decrease gallbladder prostaglandin formation and are effective in producing relief of the symptoms of gallbladder disease. In experimental cholesterol gallstone formation, prostaglandins are involved in the production of mucin, which acts as a nidus for stone formation, and cyclooxygenase inhibitors prevent the formation of experimental cholesterol gallstones. Prostaglandins have been shown to be cytoprotective in various types of experimental hepatic injury and leukotrienes have been shown to be injurious to hepatocytes and biliary tract tissues. Specific prostanoids and lipoxygenase inhibitors may be valuable in treating patients with various acute hepatic inflammatory disease processes. Continued evaluation of the role of arachidonic acid metabolites in hepatobiliary physiology and disease may lead to important new therapeutic modalities.
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PMID:Arachidonic acid metabolites in hepatobiliary physiology and disease. 266 54

Experimental evidence has recently accumulated indicating that administration of some prostaglandins (PGs), particularly those of the E series, can evoke release of glucagon by the pancreatic alpha-cells. Virtually, all the in vitro studies (isolated perfused rat pancreas, isolated guinea-pig islets) agree that PGs can increase both basal and stimulated glucagon release. On the other hand, inhibition of PG synthesis with indomethacin blocks glucagon release. In rats and in normal humans, PGE1, but not PGA2 or PGF2a, causes a progressive rise of plasma glucagon levels. While in the rat this response seems independent of the adrenergic nervous system, in man the hyperglucagonemia induced by PGE1 is easily suppressed by propranolol, suggesting an interaction between the prostaglandin and the beta-receptors of the alpha-cell. Studies with inhibitors of PG synthesis in vivo have yielded conflicting results, depending on the particular experimental protocol used and on the type of inhibitor tested. In normal humans, it seems that acetylsalicylic acid (ASA) has no effect on glucagon response to arginine, tolbutamide and insulin-induced hypoglycemia. Conversely, a stimulator of PG synthesis, such as furosemide, increases glucagon response to an arginine pulse in man. In insulin-dependent diabetics, who present an exaggerated glucagon response to stimulants, ASA fails to alter glucagon response to arginine, but completely blunts the glucagon response to salbutamol, a weak beta-2 receptor agonist. In conclusion, these observations provide evidence in support to a role for PGs, at least PGE, in the contro of glucagon release.
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PMID:Prostaglandins and the alpha-cell. 701 76

Objective: Inflammation, oxidative stress, and decreased glucagon-like peptide-1 (GLP-1) are risk factors for cognitive impairment. Dipeptidyl peptidase-4 (DPP4) was identified as a novel adipokine capable of enhancing these risk factors. Hence, we investigated the relationship between plasma DPP4 activity and impaired cognitive function in elderly Chinese population with normal glucose tolerance (NGT). Methods: We performed a cross-sectional study using data from 1229 elderly participants (60 years or older) in Guilin. Plasma DPP4 activity, oxidative stress parameters, fasting active GLP-1, and inflammatory markers were measured in all participants. Impaired cognitive function was diagnosed according to the National Institute on Aging-Alzheimer's Association workgroups criteria. Results: Participants in the upper quartile of plasma DPP4 activity had higher C-reactive protein (CRP), interleukin-6 (IL-6), 8-iso-PGF2a, nitrotyrosine, and lower GLP-1 and Montreal Cognitive Assessment (MoCA) scores compared with those in the lowest quartile (P < 0.001). The odds ratios (ORs) for increased CRP, IL-6, 8-iso-PGF2a, nitrotyrosine, and decreased active GLP-1 were higher with increasing DPP4 quartiles after adjustment for confounders (all P < 0.001). In the highest DPP4 quartile, impaired cognitive function risk was higher (OR, 2.26; 95% confidence interval, 1.36-3.76) than in the lowest quartile after adjustment for potential confounders. The risk for impaired cognitive function increased more with higher levels of DPP4 activity, nitrotyrosine and 8-iso-PGF2a (P < 0.05), but not with higher IL-6, CRP or lower GLP-1. Conclusion: Plasma DPP4 activity is significantly and independently associated with impaired cognitive function, mainly executive, in elderly Chinese population with NGT. The underlying mechanisms for this association may be partly attributed to the effect of DPP4 on oxidative stress. Plasma DPP4 activity might serve as a risk biomarker or therapeutic target for the prevention and treatment of impaired cognitive function.
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PMID:Strong Association between Plasma Dipeptidyl Peptidase-4 Activity and Impaired Cognitive Function in Elderly Population with Normal Glucose Tolerance. 2879 86