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)

Exocrine pancreatic function was evaluated by a Lundh meal test and a secretin-cholecystokinin test in 16 patients with chronic pancreatitis. B cell function was assessed by measuring the concentration of C-peptide after stimulation with oral glucose and intravenous glucagon. The Cc-peptide response to intravenous glucagon and oral glucose was closely correlated (r = 0.88, p less than 0.01). Plasma C-peptide after glucagon was significantly correlated to the post-prandial concentration of lipase (r = 0.72, p less than 0.001), amylase (r = 0.64, p less than 0.05) and to amylase output (r = 0.64, p less than 0.05). Eight out of nine patients treated with insulin had residual B cell function, but it diminished significantly with increasing duration of diabetes. We conclude that B cell function is correlated to pancreatic enzyme secretion and that patients with insulin-treated diabetes secondary to chronic pancreatitis have a residual insulin secretion similar to that of patients with Type 1 (insulin-dependent) diabetes.
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PMID:B cell function in patients with chronic pancreatitis and its relation to exocrine pancreatic function. 618 47

The effects of dietary soybean trypsin inhibitor (SBTI, Kunitz type) or repeated i.p. injections of 95% pure cholecystokinin (CCK-39) on rat pancreas were investigated in a 10-day experiment. SBTI and CKK -39 induced similar increases in pancreatic weight, which led to both cellular hypertrophy and hyperplasia. Trypsin and chymotrypsin activity increased with an increase in pancreatic weight. Amylase activity increased only after CCK-39 injection, whereas lipase activity was not affected by either SBTI or CCK-39 treatment. After both treatments, insulin content showed only a slight tendency to increase, whereas glucagon content was not different from controls. The results indicate that SBTI and CCK-39 mainly exert their effects on the exocrine pancreas in a similar but not identical manner. It is therefore suggested that SBTI is not only a potent stimulator of the secretion of CCK activity but also of other unidentified gastrointestinal factor(s).
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PMID:The effect of feeding soybean trypsin inhibitor and repeated injections of cholecystokinin on rat pancreas. 620 62

Post-heparin lipase activities were measured in normolipemic men with complaints suggestive of symptomatic coronary artery disease. A study group, who showed diffuse atherosclerotic narrowing of the coronary vessels, assessed by a quantitative computer-assisted analysis method, had a lowered hepatic lipase in comparison with a group with normal angiograms. Lipoprotein lipase was lower in the study group but well within the normal range and not statistically different. Some related hormones (cortisol, estradiol, testosterone and glucagon) were different in the two groups while others (insulin, human growth hormone, prolactin, thyroid hormones) were not. The results are discussed in view of the proposed role of hepatic lipase in the uptake of HDL-cholesterol by the liver.
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PMID:Post-heparin lipases, lipids and related hormones in men undergoing coronary arteriography to assess atherosclerosis. 635 16

Rat hearts were perfused for long periods in the presence of 14C-labeled amino acids. From these hearts, postheparin-effluent and a tissue homogenate containing lipoprotein lipase and neutral lipase, respectively, were derived. Lipolytic activity and 14C-labeled protein in both preparations were characterized by affinity chromatography, immunoprecipitation and SDS-polyacrylamide gel electrophoresis. Lipase activity and 14C-labeled protein co-eluted from heparin-Sepharose 4B at 1.2 M NaCl and were inhibited and precipitated by preincubation with anti-lipoprotein lipase gamma-globulins. Gel electrophoresis of both preparations showed the presence of 14C-labeled protein with a molecular weight of 35 000. These data strongly suggest similarity between lipoprotein lipase and neutral lipase and their possible precursor-product relationship and indicate that during perfusion continuous synthesis, secretion and vascular binding of lipase molecules occur. Cycloheximide perfusion induced a dramatic decrease of lipoprotein lipase and neutral lipase activity, indicating a half-life of less than 90 min for both enzymes. Tunicamycin present during perfusion also induced a drop in lipoprotein lipase and tissue neutral lipase activity, indicating that glycosylation is necessary for secretion of lipoprotein lipase. Long-term perfusion of rat hearts in the presence of norepinephrine, glucagon or tyrosine leads to reciprocal alterations in lipoprotein lipase and neutral lipase activities, i.e., lipoprotein lipase activity increased and neutral lipase activity decreased, whereas total lipase activity (lipoprotein lipase + neutral lipase) remained unaltered. During perfusion in the presence of insulin, no net change in lipase activities was observed. Also, insulin did not affect the glucagon-induced inverse effects on either lipase activity. The reciprocal changes in lipase activities occurring during norepinephrine perfusion were hampered by colchicine and propranolol, pointing towards beta-receptor and microtubular mediation of tissue lipase processing and endothelial binding. Our data suggest that the tissue flux and vascular binding of lipase protein may be important sites of hormonal regulation of lipoprotein lipase homeostasis.
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PMID:Effects of hormones, amino acids and specific inhibitors on rat heart heparin-releasable lipoprotein lipase and tissue neutral lipase activities during long-term perfusion. 637 31

The alkaline, heparin-releasable lipoprotein lipase (LPL) activity of isolated, perfused rat hearts was compared with the residual neutral lipase (NL) activity detectable in the post nuclear supernatant (PNS) from a tissue homogenate. Both enzyme activities were increased by serum, heparin and apolipoprotein CII, inhibited by high salt concentrations and by immunotitration with an anti-LPL gamma-globulin fraction. Protamine sulphate from saline liver inhibited LPL activity and the NL activity only in the absence of serum. Incubation of the PNS NL under classic conditions of hormonal stimulation (by phosphorylation) did not alter its activity and upon short-term preperfusion of the hearts with norepinephrine and glucagon also unchanged LPL and NL activities were measured. Our experiments are indicative of a possible similarity between vascular LPL and tissue NL and show that the lipase activities are not sensitive towards hormonal stimulation.
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PMID:Comparison of heparin-releasable lipase and tissue neutral lipase activity of rat heart. 667 39

Hormonal and metabolic regulation of endogenous triglyceride hydrolysis was studied in triglyceride-enriched hearts obtained from rats fed 3 days with a trierucate-rich diet. Endogenous lipolysis was determined by measuring glycerol release during in vitro perfusion of the hearts. It appeared that there was a direct relation between the contractile state of the heart, the rate of glycerol release in the coronary effluent and the Ca2+ concentration in the perfusion medium. During Ca2+-free perfusion, 2,4-dinitrophenol stimulated oleate oxidation and this, as well as the addition of 2 x 10(-7) M glucagon, induced a marked stimulation of lipolysis. Insulin did not affect glucagon- and norepinphrine-stimulated lipolysis during substrate-free perfusion. The presented experiments point out that in lipid-enriched rat hearts the activity of the tissue lipase may be controlled by the rate of beta-oxidation and re-esterification of the liberated fatty acid, as well as by a shift to utilization of carbohydrate instead of fatty acids for energy supply.
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PMID:Control of lipolysis in triglyceride-enriched rat hearts. 702 May 66

Nasogastric suction, glucagon, and cimetidine are proposed treatments for human acute pancreatic because they may reduce gastric acid and exocrine pancreatic secretion. However, the functional status of gastric and pancreatic secretion during human acute pancreatitis is unknown. Thus, we compared the effects of nasogastric suction, intravenous glucagon (5 microgram/kg per hour), and cimetidine (2 mg/kg per hour) on the output of acid and pancreatic enzymes and the clinical course of human acute pancreatitis. In three subjects with acute alcoholic pancreatitis, gastric acid secretion was increased above normal and was decreased by glucagon and cimetidine used alone and in combination. In two of the three patients, duodenal output of trypsin and lipase was normal or increased and was reduced by glucagon and cimetidine given alone or in combination. Twenty patients with documented acute pancreatitis randomly received treatment with nasogastric suction, cimetidine alone, or the combination of cimetidine and glucagon. Four of the five complications observed during the trial occurred in the combination-treatment group (P less than 0.05). Administration of cimetidine alone or with glucagon did not improve the outcome when compared with nasogastric suction.
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PMID:A prospective study of the antisecretory and therapeutic effects of cimetidine and glucagon in human acute pancreatitis. 702 37

Triacylglycerol lipase activities of homogenates and subcellular fractions of rat liver were measured under optimal conditions at pH 7.5 using emulsified tri[1-14C]oleoylglycerol as substrate. Twenty-four hr after administration of streptozotocin, hepatic alkaline lipase activity was 39% of normal, and this lower level of activity was observed at 72 hr and 7 days, after streptozotocin injection. After 24 hr of starvation, lipase activity also was significantly lower (35%) than normal. Insulin (35 U regular/kg body weight) had no acute (90 min) effect on the hepatic lipase activity of either normal or diabetic rats. Chronic insulin administration (4 subcutaneous injections of 10 U protamine zinc insulin/kg at 16-hr intervals) to normal rats provoked a 40% increase in hepatic lipase activity. Diabetic rats given the same insulin treatment showed lipase activity that was significantly higher (155%) than normal. Lipase activity fell to 65% of normal when insulin was withheld (32 hr) from diabetic rats given chronic insulin therapy. Intracardial injection of glucagon (1 mg/kg) into normal rats had no acute (30 min) effect on hepatic alkaline lipase activity. Hepatic alkaline lipase activity varied independently from the concentrations of either glucose or triacylglycerol in the plasma. However, there was an apparent negative correlation between this lipase activity and the concentration of fatty acids in the plasma; lipase activity was highest when fatty acid concentrations were lowest, and lowest when fatty acid concentrations were elevated. From these data we conclude: 1) changes in hepatic alkaline lipase activity ware provoked by chronic, but not acute, alteration of the hormonal and metabolic status of the rat, and 2) changes in hepatic alkaline lipase activity may be mediated through changes in the levels of circulating fatty acids presented to the liver, but the effect is not an immediate one.
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PMID:Hepatic triacylglycerol lipase activities after induction of diabetes and administration of insulin or glucagon. 704 62

While pancreatic metaplasia has been observed in gastric mucosa of patients with chronic gastritis, it has not been described in ectopic gastric mucosa. We have identified focal clusters of cells resembling pancreatic acinar cells (CPACs) in 11 of 350 biopsies of Barrett's mucosa from 120 patients with Barrett's esophagus enrolled in a clinical efficacy trial of omeprazole versus ranitidine for treatment of gastroesophageal reflux disease. Three additional cases from our surgical files were also studied. Immunoreactivity for trypsin and chymotrypsin was present in the CPACs of all 14 cases, while stains for alpha-amylase and lipase were each positive in 12 of 13. A few cells in the CPACs were also positive for chomogranins (12 of 13 cases), serotonin (seven of 13 cases), somatostatin (three of 12), gastrin (four of 11), and pancreatic polypeptide (two of 13). No staining was seen for insulin or glucagon. Ultrastructural studies performed in one case showed features of pancreatic exocrine and endocrine (PP-type) cells in cells within CPACs. These results collectively indicate that the CPACs are aggregates of true pancreatic acinar cells admixed with a few endocrine cells. This pancreatic parenchyma in Barrett's mucosa is most likely of metaplastic origin and could be derived from the transitional zone cells or from pluripotent stem cells in the esophageal mucosa or from metaplasia of mucus cells. While the development of pancreatic metaplasia in Barrett's esophagus appears to be unrelated to drug therapy, the clinical relevance of this distinctive histological finding needs further investigation.
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PMID:Pancreatic metaplasia in Barrett's esophagus. An immunohistochemical study. 757 75

It is well known that oral administration of camostate induces hyperplasia and hypertrophy of the rat pancreas. It is not clear, however, whether pancreatic hormone and enzyme secretion are affected by camostate treatment. In rats, daily administration of 200 mg camostate/kg b. wt for 14 days significantly increased pancreatic weight and pancreatic content of DNA, protein, amylase, lipase, trypsin and chymotrypsin, as well as the amount of insulin, glucagon and somatostatin. In the intact animal, blood glucose levels and serum concentrations of insulin and glucagon in response to an oral glucose load were not impaired after camostate treatment. In the isolated perfused pancreas, however, insulin and glucagon secretions were reduced, whereas somatostatin release was not affected. The volume of pancreatic juice produced by the unstimulated isolated perfused organ, as well as protein and enzyme secretion, were increased after camostate treatment. Likewise, the isolated perfused pancreas from camostate-treated rats secreted a larger volume of pancreatic juice and more protein in response to cholecystokinin (CCK), while enzyme secretion was affected in a non-parallel manner: amylase release was markedly reduced, lipase release was unchanged, and release of trypsin and chymotrypsin was increased.
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PMID:Endocrine and exocrine pancreatic function after camostate-induced growth of the organ. 760 95


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