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)

Hormone-sensitive lipase and cholesterol ester hydrolase of chicken adipose tissue were markedly activated by adenosine 3':5'-monophosphate (cAMP)-dependent protein kinase (on the average, 235 to 275%; occasionally as much as 1000%). Diglyceride and monoglyceride hydrolases were also activated, but to a lesser extent (60 to 87%). The activation of all four hydrolases was inhibited by protein kinase inhibitor and reversed by the addition of exogenous protein kinase. Following activation by cAMP-dependent protein kinase, all four hydrolases were deactivated in a Mg2+-dependent reaction and then reactivated to or near initial levels on incubation with cAMP and Mg2+-ATP. The reversible deactivation is assumed to reflect activity of one or more protein phosphatases. The maximum activation obtainable for the four hydrolases decreased when the tissue had been previously exposed to glucagon, indicating that the glucagon-induced activation was probably similar to or identical with the activation demonstrated in cell-free preparations. The pH optima for the four hydrolase activities were similar (7.13 to 7.38). Although the absolute activities and relative degrees of kinase activation differed according to the particular emulsified substrates used, the results do not rule out the possibility that all four hydrolase activities are referable to a single hormone-sensitive hydrolase. Hormone-sensitive acyl hydrolases were separated from lipoprotein lipase by heparin-Sepharose affinity chromatography. Lipoprotein lipase was active against triolein, diolein, and monoolein, but not cholesterol oleate. Incubation of lipoprotein lipase with exogenous protein kinase, cAMP, and Mg2+ATP had no effect on any of the three hydrolase activities. Lipoprotein lipase was further purified to homogeneity and used to prepare antiserum in rabbits. The immunoglobin G fraction from these antisera completely inhibited lipoprotein lipase eluted from heparin-Sepharose columns. However, the hormone-sensitive hydrolase activities (not retained on heparin-Sepharose affinity chromatography) were not inhibited by anti-lipoprotein lipase immunoglobin G, and anti-lopoprotein lipase immunoglobin G did not affect the activation process in crude fractions. Thus, hormone-sensitive lipase and lipoprotein lipase, functionally distinct enzymes, have been physically resolved and immunochemically distinguished. Apparently lipoprotein lipase activity is not regulated, at least directly, by cAMP-dependent protein kinase.
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PMID:Triglyceride, diglyceride, monoglyceride, and cholesterol ester hydrolases in chicken adipose tissue activated by adenosine 3':5'-Monophosphate-dependent protein kinase. Chromatographic resolution and immunochemical differentiation from lipoprotein lipase. 0 45

An adenylate cyclase activity (AC) was found in guinea pig brown adipose tissue (BAT), since the tissue's apparition. This enzymatic activity increased during the development and showed high values at the end of gestation. An increase of AC units per cell was observed, in addition to the cell multiplication. A norepinephrine stimulation of AC activity was observed at the end of gestation : this regulating action disappeared in the first days of extrauterine life. Neither glucagon nor ACTH had any regulating role upon AC activity during fetal and newborn life. The basal lipolytic activity which was observed in BAT of fetuses (61rst day) and neonate dramatically around the 15th day. A potent lipolysis activation by norepinephrine was observed, but only after birth. The correlation observed between these enzymatic activities in presence of norepinephrine seems to indicate that the AC/lipase system was involved in the neonatal thermogenesis of guinea pigs.
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PMID:[Adenylate cyclase/Lipase. Hormone receptor induction]. 17 89

Plasma lipids and lipoproteins were studied in a group of chronic uraemia patients some of whom were maintained by regular haemodialysis. Compared with healthy individuals, there was a significant increase in plasma triglycerides and in the prebeta-1- and prebeta-2-lipoprotein plasma concentrations. There was no difference between dialyzed and undialyzed patients. Carbohydrate intake was normal, basal plasma insulin and free fatty acid levels were within the normal range. There was no correlation between plasma triglyceride levels and the degree of hypoalbuminaemia, the latter being marked in 30% of the patient. Basal plasma glucagon levels were very high in nearly all dialyzed patients and post-heparin lipoprotein-lipase activity was very low in dialyzed patients. In our experience, regular haemodialysis for 32 weeks did not improve hypertriglyceridaemia.
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PMID:Lipids and lipoproteins in chronic uraemia. A study of the influence of regular haemodialysis. 17 95

The procedure of Berry and Friend for isolation of intact hepatocytes has been adapted to mouse livers. The ultrastructure of these cells was satisfactorily preserved. Isolated mouse hepatocytes secreted proteins and triacylglycerols. These secretory processes were inhibited by colchicine, indicating a likely involvement of the microtubular system for their normal occurrence. Ultracentrifugation of medium incubated with hepatocytes, followed by electrophoresis and electron microscopic examination of the floating fraction (density less than 1.006) allowed to conclude that secreted triacylglycerols were very low density lipoproteins. Glycogenolysis and lipogenesis were stimulated or inhibited, respectively, by low concentrations of glucagon (10(-10) M). Other metabolic parameters were influenced by the hormone but were less sensitive to its action. Inhibition of lipogenesis by glucagon was associated with a decrease in acetyl CoA carboxylase activity. This decrease does not appear to be related to intracellular fatty acyl-CoA accumulation secondary to hepatic lipase activation by the hormone. Insulin was effective alone or counteracted glucagon effects on lipogenesis or glycogenolysis only when exposure of cells to collagenase was held minimal. This suggests that, during isolation of hepatocytes, insulin receptors may, for unknown reasons, be more fragile than those of glucagon.
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PMID:Secretory processes, carbohydrate and lipid metabolism in isolated mouse hepatocytes. Aspects of regulation by glucagon and insulin. 17 77

Lipoprotein-lipase activity was determined in tissue from the skeletal muscle of the leg and the subcutaneous adipose tissue of the abdomen in fourteen patients before and after 1 month of clofibrate administration. The concentrations of serum triglycerides decreased by, on the average, 37% in a group of thirteen patients which mainly consisted of subjects with type-IV hyperlipoproteinaemia. Clofibrate administration was associated with an average increase of the skeletal muscle-tissue lipoprotein-lipase activity of 50% (P less than 0.005). There was a significant correlation between the percentage changes in skeletal muscle-tissue lipoprotein-lipase activity and those of the triglycerides concentrations and the K2-values in an intravenous fat tolerance test during clofibrate treatment. Adipose-tissue lipoprotein-lipase activity did not change significantly. One patient with type-I hyperlipoproteinaemia had very low values of skeletal muscle-tissue lipoprotein-lipase activity and moderately low adipose-tissue lipoprotein-lipase activity. In this patient, neither the tissue lipoprotein-lipase activity nor the triglycerides concentration changed during clofibrate therapy. Fasting serum insulin concentrations decreased significantly during clofibrate administration and the percentage decrease was significantly correlated to the percentage increase of skeletal-muscle lipoprotein-lipase activity. It is suggested that the lowering of insulin levels is a possible mechanism through which glucagon activity is enhanced and this may increase skeletal muscle-tissue lipoprotein-lipase activity.
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PMID:Increase of the lipoprotein-lipase activity in human skeletal muscle during clofibrate administration. 41 37

Metabolic studies of a 9-year-old girl with primary type V hyperlipoproteinemia demonstrated normal glucose tolerance, plasma insulin and glucagon responses to stimuli, and serum uric acid level. Fasting plasma triglyceride levels rapidly increased when the patient received a diet containing 40% of the total calories as fat and rapidly decreased on a 10% fat diet. Hepatic and nonhepatic lipase activities in postheparin plasma were normal, thus excluding type I hyperlipoproteinemia. Because of the potential complication of acute pancreatitis in this disorder, early diagnosis and prompt institution of diet therapy is important.
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PMID:Primary type V hyperlipoproteinemia in childhood. 57 87

The subject of investigations was the influence of some endogenic substances: ions (K+ and Ca++), amines (serotonin, histamine and acetylcholine) and hormones (hydrocortisone and glucagon) on the lipase release from pancreatic granules (zymogen and lysosomes) of control and irradiated rats (800 R=24 hours). The decrease of enzyme release under the influence of hydrocortisone (both concentrations: 10(-6) and 10(-8) M), Ca++ ions, serotonin, histamine and acetylcholine after their administration in greater concentration (10(-6) M) was stated. Smaller concentrations of these substances evoked the transitory enhancement of enzyme activity. K+ ions and glucagon increased the lipase release (both concentrations). In the fraction of organelles from irradiated rats the action of K+ ions, glucagon and acetylcholine was diminished or abolished, while the inhibitory effectiveness (of greater concentrations) of Ca++ ions, serotonin, histamine and hydrocortisone was maintained.
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PMID:Investigations on the modification of postirradiation pancreatic lipase activity by some endo- or exogenic factors. Part II. The influence of some ions, biogenic amines and hormones. 66 54

Sixteen healthy subjects, 7 females and 9 males, with a mean age of 25 years (range 22--29 years), were studied in the fasting state in the morning and 8 h later after partaking of breakfast, lunch and two small meals. The lipoprotein-lipase activity in the adipose tissue increased significantly from 80 +/- 32 to 117 +/- 61 nmol fatty acid released per gram and minute (nmol FA/g/min), whereas in skeletal-muscle tissue it decreased significantly from 25 +/- 11 to 17 +/- 9 nmol FA/g/min. The concentration of serum triglycerides increased significantly from 0.93 +/- 0.18 mmol/l (mean +/- SD) in the fasting state to 1.57 +/- 0.64 mmol/l in the fed state. In the fasting state the lipoprotein-lipase activity of skeletal muscle was inversely related to the ratio between the concentrations of insulin and glucagon.
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PMID:Lipoprotein-lipase activity in human skeletal muscle and adipose tissue in the fasting and the fed states. 67 12

CFY male rats anaesthetized with pentobarbital were used in different groups for inducing acute pancreatitis by the retrograde injection either of 1 mg elastase, 5 mg trypsin, 4 mg lysolecithin, 10 mg Na-taurocholate in 0.2 ml volume or of 0.3 m. sunflower oil. In each group laparatomized animals served for control. The animals with pancreatitis were treated either with 15 mug/b.w.kg/hour glucagon or with physiological saline for 72 hours. Twenty-four and 72 hours after inducing pancreatitis glucagon did not influence the significant fall in blood pressure elicited by the intraductal injection of trypsin or elastase or in the plasma calcium level in pancreatitis induced by trypsin or sunflower oil. Neither did glucagon affect the significant increase of plasma lipase activity in pancreatitis induced by trypsin or taurocholate. It also failed to reduce the 24-hour mortality rate and the extension of fat tissue necrosis in the abdominal cavity of pancreatitic animals. In contrast, glucagon treatment significantly reduced the amount of abdominal exudate associated with bile salt induced pancreatitis and, probably due to its pancreatic blood flow increasing effect, seemed to moderate the degree of tissue damage elicited in the pancreas by detergents such as taurocholate or lysolecithin.
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PMID:Glucagon treatment of experimental acute pancreatitis. 123 17

Lipolytic activity of fish (Hoplias malabaricus), toad (Bufo paracnemis), and snake (Philodryas patagoniensis) adipose tissue was investigated in vivo and in vitro. Catecholamines or glucagon did not affect the release of free fatty acids (FFA) by incubated fish and toad adipose tissue. Catecholamines also failed to activate snake adipose tissue lipolysis, which even decreased in the presence of epinephrine. However, glucagon stimulated both the lipolytic activity of reptilian tissue in vitro and the mobilization of FFA to plasma when administered to snakes in vivo. The release of FFA from incubated fish, amphibian, and reptilian adipose tissue increased markedly in the presence of cAMP or xanthine derivatives, inhibitors of phosphodiesterase. Forskolin or fluoride, activators of specific components of the adenylate cyclase system, strongly stimulated toad adipose tissue lipolysis. The data suggest that adipocyte triacylglycerol lipase of ectotherm vertebrates is activated by a cAMP-mediated phosphorylation and that the organization of the membrane-bound adenylate cyclase system is similar to that of mammals.
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PMID:Control of adipose tissue lipolysis in ectotherm vertebrates. 132 67


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