Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.9 (glucose-6-phosphatase)
3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activities of hexokinase, glucokinase, phosphofructokinase, glucose-6-phosphate dehydrogenase, glucose-6-phosphatase, and fructose-1,6-diphosphatase were determined in loach embryos developed in solutions of insulin, hydrocortisone, estrone and thyroxin at different stages of embryogenesis. Glucokinase and fructose-1,6-diphosphatase activties are shown not to change markedly under the influence of the above-mentioned hormones. During some periods of early development the hexokinase activity is inhibited by insulin, estrone and thyroxin. The glucose-6-phosphate dehydrogenase activity is suppressed by each of the used hormones at all the stages of early embryogenesis while the glocose-6-phosphatase activity decreased only under the influence of insulin at the cleavage, blastula and gastrula stages. Insulin increased the activity of phosphofructokinase at the cleavage, blastula and early gastrula stages and hydrocortisone, estrone and thyroxine during certain periods of these stages. From middle gastrula two last hormones decreased the phosphofructokinase activity in the loach embryos.
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PMID:[Activity of carbohydrate metabolism enzymes in loach embryos under the influence of hormones]. 19 80

Hyperinsulinemia was produced in fetal rhesus monkeys for 21 days in the last third of gestation by subcutaneous pork insulin injected at 19 U a day. Plasma insulin concentrations in treated fetuses (N = 4) were 3525 microU/ml. There was no difference in paired pre- and post-treatment fetal plasma glucose concentration. Activity of the hepatic enzymes that promote glucose utilization (glucokinase and hexokinase) and glycolysis (phosphofructokinase, pyruvate kinase, and pyruvate dehydrogenase) was unaffected. Similarly, glycogen metabolism enzymes (active and inactive synthase and phosphorylase) were unaltered. Two gluconeogenic enzymes (PEPCK and glucose-6-phosphatase) were diminished in the treated group compared with controls. Fetal hyperinsulinemia enhanced lipogenic and NADPH-producing enzyme activities, as evidenced by a twofold increase in fatty acid synthase and in citrate cleavage enzyme activity. Malic enzyme was absent. Hyperinsulinemia with euglycemia (1) increases the activity of enzymes that participate in lipogenesis, (2) decreases some of those controlling gluconeogenesis, and (3) has no effect on the enzymes of glycolysis.
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PMID:Chronic hyperinsulinemia in the fetal rhesus monkey: effects on hepatic enzymes active in lipogenesis and carbohydrate metabolism. 22 50

Effects of pioglitazone (5-[4-[2-(5-etyl-2-pyridyl)ethoxy] benzyl]-2,4-thiazolidinedione, AD-4833, also known as U-72, 107E) on peripheral and hepatic insulin resistance were examined using genetically obese-hyperglycemic rats, Wistar fatty. Pioglitazone was administered to fatty rats (3 mg/kg/d) and lean rats (10 mg/kg/d) for 6 days. Pioglitazone decreased hyperglycemia and hypertriglyceridemia without affecting hyperinsulinemia in the fatty rats, and significantly reduced plasma levels of triglyceride and insulin without altering normoglycemia in the lean rats. The same rats were subjected to an isotopic method combined with a euglycemic clamp technique for assessing insulin sensitivity in hepatic glucose production (HGP) and peripheral glucose utilization (PGU). HGP decreased and PGU increased in response to infused insulin in the lean rats but did not in the fatty rats, indicating that insulin resistance was present in the liver and peripheral tissues of the fatty rats. Treatment with pioglitazone restored the responses of HGP and PGU to infused insulin in the fatty rats, but did not produce any changes in the lean rats. When the same levels of glycemia and insulinemia were established by 480 mU/h of insulin in both treated and control fatty groups, PGU was 1.5-fold higher and HGP was 3-fold lower in the pioglitazone treated group. Pioglitazone also corrected the abnormality in hepatic enzyme regulation by insulin of the fatty rats: glucose-6-phosphatase decreased and glucokinase increased, suggesting the increased response of the liver to insulin and the resultant suppression of HGP. Therefore, pioglitazone is expected to be useful for treating abnormal glucose and lipid metabolism in non-insulin-dependent diabetes mellitus through reducing insulin resistance of the peripheral tissues and liver.
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PMID:Effects of pioglitazone on hepatic and peripheral insulin resistance in Wistar fatty rats. 219 15

The present studies were designed to clarify the contribution of the liver to the development of hyperglycemia in Wistar fatty rats. The hepatic activities of insulin-inducible enzymes involved in glycolysis (glucokinase; GK and pyruvate kinase) and lipogenesis (glucose-6-phosphate dehydrogenase), were higher in fatty rats than in lean rats at 4 and 8 weeks of age because of the higher insulin levels in the former. Thereafter, the GK activities of fatty rats decreased slightly in spite of severe hyperinsulinemia, and did not differ from those of lean rats. In addition, fatty rats had higher levels of insulin-suppressible gluconeogenic enzymes, glucose-6-phosphatase (G6Pase) and fructose-1, 6-diphosphatase. These findings indicate that the hepatic enzymes of fatty rats are resistant to insulin. This postulation was supported by the fact that the hepatic enzyme activities of fatty rats showed a lower response to changes in plasma insulin levels produced by fasting and refeeding. The G6Pase/GK ratio, which indicates net glucose handling in the liver, increased in fatty rats and decreased in lean rats with advancing age, suggesting that hepatic glucose production in fatty rats becomes dominant with advancing age. The changes in hepatic glycolytic intermediates supported this suggestion; the glycolytic steps both from glucose to glucose-6-phosphate and from phospho-enolpyruvate to pyruvate in fatty rats were accelerated at 5 weeks of age, but suppressed at 12 weeks of age. These results indicate that insulin resistance in the hepatic enzyme regulation may contribute to the development of hyperglycemia in Wistar fatty rats.
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PMID:Pathogenesis of hyperglycemia in genetically obese-hyperglycemic rats, Wistar fatty: presence of hepatic insulin resistance. 254 49

Eight-week-old, female Wistar fatty rats and their lean littermates were given a 30% sucrose solution in addition to a laboratory chow diet and water for 7 weeks. The fatty rats were hyperinsulinemic and hyperlipidemic, but normoglycemic when they drank only water. The hepatic activities of insulin-inducible glucokinase (GK), pyruvate kinase (PK), and malic enzyme (ME) were higher in the fatty rats than in the lean rats, whereas the insulin-suppressible glucose-6-phosphatase (G6Pase) activity was similar in both types of rats, indicating the normal response of hepatic enzymes to hyperinsulinemia in the fatty rats. When they drank the sucrose solution, the fatty rats, but not the lean rats, developed hyperglycemia over 200 mg/dl. Plasma insulin and triglyceride concentrations increased in both types of rats. Although the hepatic activities of GK, PK, and ME in the lean rats, and PK and ME in the fatty rats increased in response to the increase in plasma insulin, GK activity decreased in the fatty rats. On the other hand, G6Pase activity increased in both types of rats. As a result, the G6Pase/GK ratio, which may reflect net glucose handling in the liver, increased twofold in the fatty rats, but did not alter in the lean rats. From these findings, we conclude that sucrose ingestion induces an increase in hepatic glucose production through derangement of the hepatic enzyme profile and that the resultant decrease in hepatic glucose handling may be one of the pathogenic factors participating in the development of hyperglycemia in Wistar fatty rats.
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PMID:Derangement in hepatic enzymes caused by sucrose-drinking and its implication for the development of hyperglycemia in female Wistar fatty rats. 267 49

Salmon (Oncorhynchus kisutch) somatostatin (sSS; 4 or 8 ng/g body wt) or synthetic Gillichthys urotensin II (UII; 2 or 4 ng/g body wt) were injected intraperitoneally into juvenile freshwater coho salmon. Both sSS and UII caused a dose-dependent increase in plasma free fatty acids (FFA) which diminished with time. sSS induced an initial (1 hr) transient hyperglycemia. By contrast, UII tended to induce hypoglycemia, this effect being significant 5 hr after injection of the higher dose. Both sSS and UII depressed plasma insulin titers 1 hr after injection. By 3 hr, the sSS-associated insulin depression was no longer observed. UII treatment induced a hyperinsulinemia which was present 3 and 5 hr after peptide administration. Although no decreases in liver total lipid concentration or in mesenteric fat total tissue mass were observed, lipolytic enzyme activity within each depot was significantly enhanced by both peptides. Neither sSS nor UII altered 3H2O incorporation into fatty acids or neutral lipids. However, enhanced lipogenesis, particularly by UII, was indicated by increased NADPH production resulting from glucose-6-phosphate dehydrogenase activity. Both sSS and UII enhanced glucose mobilization, as indicated by decreased liver glycogen content and increased liver glucose-6-phosphatase activity. UII, but not sSS, stimulated glycogen synthetase activity. These results suggest that both sSS and UII stimulate hyperlipidemia by enhancing depot lipase activity and that although both factors are potentially gluconeogenetic, sSS seems to be glycogenolytic and hyperglycemic, whereas UII may channel glucose to FFA synthesis.
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PMID:Effects of somatostatin-25 and urotensin II on lipid and carbohydrate metabolism of coho salmon, Oncorhynchus kisutch. 288 97

The effect of fetal hypoglycemia and hypoinsulinemia on fetal rat hepatic glucose-6-phosphatase activity was studied. Fetal hypoglycemia and hypoinsulinemia were produced by inducing maternal hyperinsulinemia and hypoglycemia secondary to the exogenous administration of insulin via implantation of osmotically driven minipumps on day 15 of gestation into 15 experimental animals. 13 animals served as sham-operated controls. Cesarean sections were performed on day 20 or 21 of gestation under pentobarbital anesthesia. Liver glucose-6-phosphatase activity was increased in the hypoinsulinemic fetuses. In contrast, the hyperinsulinemic mothers had suppressed hepatic glucose-6-phosphatase activity. Hypoinsulinemia would appear to be the primary stimulus for enhanced fetal glucose-6-phosphatase in this model.
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PMID:Induction in utero of hepatic glucose-6-phosphatase by fetal hypoinsulinemia. 298 86

Carbohydrate intolerance was investigated in 8 alcoholics with liver cirrhosis and in controls. Indices of carbohydrate metabolism, glucose and insulin levels after glucose loading, were compared with glucose phosphorylating (glucokinase, hexokinase) and releasing (glucose-6-phosphatase) enzymes. Comparison was also made with pericellular collagen in liver biopsies and with insulin sensitivity assessed by the euglycemic clamp technique and with conventional liver function tests including oral antipyrine test. Glucokinase activity was low or absent, hexokinase activity increased and the GK/HK ratio reduced. Glucose-6-phosphatase activity was lowered and insulin sensitivity decreased. Pericellular collagen was increased (P less than 0.001) and related to the fasting glucose (r0.593) and insulin levels (r0.526). Blood glucose was related to antipyrine metabolism (r-0.727) but not to the other liver tests. Glucose intolerance in cirrhosis seems to be associated with reduced glucose phosphorylating and liberating enzyme activities. Hyperinsulinaemia, developing secondarily, may then lead to insulin resistance.
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PMID:Carbohydrate intolerance associated with reduced hepatic glucose phosphorylating and releasing enzyme activities and peripheral insulin resistance in alcoholics with liver cirrhosis. 299 23

We studied the effects of insulin and glucagon on energy and carbohydrate metabolism of rat hepatocytes in primary culture. The aim of this study is to elucidate the mechanism of the synergistic action of insulin and glucagon and to evaluate the combined effects of these hormones on liver injury. Insulin increased the level of adenosine triphosphate in hepatocytes in the presence of glucagon. Insulin increased the activities of glucokinase (EC 2.7.1.1), phosphofructokinase (EC 2.7.1.11), pyruvate kinase (EC 2.7.1.40) type L and glucose 6-phosphate dehydrogenase (EC 1.1.1.49). Glucagon had no antagonistic effect on these increases. Glucagon increased the activity of glucose 6-phosphate (EC 3.1.3.9) (G6Pase) in the presence or absence of insulin, while insulin had no effects on the levels of G6Pase and fructose 1,6-bisphosphatase (EC 3.1.3.11) in the presence or absence of glucagon. Metabolite analysis of cultured hepatocytes indicated that insulin and glucagon have antagonistic effects on the glycolytic activity of hepatocytes. These combined effects of insulin and glucagon may partially explain the preventive effects of these hormones on liver injury.
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PMID:Effects of insulin and glucagon on energy and carbohydrate metabolism of rat hepatocytes in primary culture. 306 23

Chronic fetal hyperinsulinemia, similar to that found in human infants of diabetic mothers, was produced in fetal rhesus monkeys during the latter third of gestation. Fetal plasma glucose and amino acid concentrations were found to be inversely logarithmically correlated with plasma insulin concentration. Fetal plasma glucagon concentrations were suppressed by hyperinsulinemia. Fetal plasma erythropoietin concentrations were increased by hyperinsulinemia in a dose/response manner. The activity of the hepatic gluconeogenic enzymes glucose-6-phosphatase and total phosphoenolpyruvate carboxykinase were reduced by hyperinsulinemia. Fatty acid synthase complex activity was, in contrast, increased by hyperinsulinemia while citrate cleavage enzyme and glucose-6-phosphate dehydrogenase were only increased when supraphysiologic hyperinsulinemia was produced. This model provides an opportunity to study the metabolic effects of hyperinsulinemia separate from those of hyperglycemia on the primate fetus, making it a useful model for the study of fetal pathologic conditions in diabetic pregnancies.
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PMID:Chronic hyperinsulinemia in the fetal rhesus monkey: effects of physiologic hyperinsulinemia on fetal substrates, hormones, and hepatic enzymes. 638 23


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