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 present study investigated the changes in carbohydrate metabolism of eggs of the whitefish, Coregonus spp. during embryogenesis (unfertilized eggs to embryos in the eyed stage). Occurrence of glycolysis was proved by activities of phosphofructokinase (PFK-1) and pyruvate kinase and by decreasing levels of hexose, pentose phosphate pathway by transaldolase (non-oxidative path) and glucose-6-phosphate dehydrogenase activities (oxidative path) and by increasing ribose levels, fructose synthesis (polyol pathway) by sorbitol dehydrogenase activities, gluconeogenesis by activities of glucose-6-phosphatase. Glycolysis and pentose phosphate pathway had highest activities up to the epiboly stage, gluconeogenesis from epiboly stage to the eyed embryo stage. Coregonus spp. eggs contained hexoses, ketoses, 6-deoxyhexoses, heptoses and uronic acids with hexoses, ketoses, and 6-deoxysugars occurring free and in bound form. Hexoses were found in highest quantities, followed by ketoses, and 6-deoxyhexoses. Levels of these compounds changed in a specific way during embryogenesis. During all investigated stages of embryogenesis, the levels of ribose, heptose, and ketose were correlated with the percentage of eyed stage embryos developing out of the fertilized eggs (egg viability). In distinct embryonic stages, the levels of hexoses and 6-deoxyhexoses and the activities of glucose-6-phosphatase were also correlated with egg quality. This ascertains the importance of carbohydrate metabolism for developing eggs.
Comp Biochem Physiol B Biochem Mol Biol 2005 Sep
PMID:Carbohydrate metabolism of eggs of the whitefish, Coregonus spp. during embryogenesis and its relationship with egg quality. 1604 62

Fenugreek and Balanites are two plants commonly used in Egyptian folk medicine as hypoglycemic agents. In the present study, the effects of 21 days oral administration of Fenugreek seed and Balanites fruit extracts (1.5 g/kg bw) on the liver and kidney glycogen content and on some key liver enzymes of carbohydrate metabolism in STZ-diabetic rats were studied. In addition, the effects of these two plant extracts on the intestinal alpha-amylase activity in vitro and starch digestion and absorption in vivo were also examined. Results indicated that single injection of STZ (50 mg/kg bw) caused 5-folds increase in the blood glucose level, 80% reduction in serum insulin level, 58% decrease in liver glycogen and 7-folds increase in kidney glycogen content as compared to the normal levels. The activity of glucose-6-phosphatase was markedly increased, whereas, the activities of both glucose-6-phosphate dehydrogenase and phospho-fructokinase were significantly decreased in the diabetic rat liver. Administration of Fenugreek extract to STZ-diabetic rats reduced blood glucose level by 58%, restored liver glycogen content and significantly decreased kidney glycogen as well as liver glucose-6-phosphatase activity. Meanwhile, Balanites extract reduced blood glucose level by 24% and significantly decreased liver glucose-6-phosphatase activity in diabetic rats. On the other hand, our results demonstrated that both the Fenugreek and Balanites extracts were able to in vitro inhibit alpha-amylase activity in dose-dependent manner. Fenugreek was more potent inhibitor than Balanites. This inhibition was reversed by increasing substrate concentration in a pattern which complies well with the effect of competitive inhibitors. Furthermore, this in vitro inhibition was confirmed by in vivo suppression of starch digestion and absorption induced by both plant extracts in normal rats. These findings suggest that the hypoglycemic effect of Fenugreek and Balanites is mediated through insulinomimetic effect as well as inhibition of intestinal alpha-amylase activity.
Mol Cell Biochem 2006 Jan
PMID:Biochemical study of the anti-diabetic action of the Egyptian plants fenugreek and balanites. 1632 70

We determined the effect of dietary starch on growth performance and feed utilization in European sea bass juveniles. Data on the dietary regulation of key hepatic enzymes of the glycolytic, gluconeogenic, lipogenic and amino acid metabolic pathways (hexokinase, HK; glucokinase, GK; pyruvate kinase, PK; fructose-1,6-bisphosphatase, FBPase; glucose-6-phosphatase, G6Pase; glucose-6-phosphate dehydrogenase, G6PD; alanine aminotransferase, ALAT; aspartate aminotransferase, ASAT and glutamate dehydrogenase, GDH) were also measured. Five isonitrogenous (48% crude protein) and isolipidic (14% crude lipids) diets were formulated to contain 10% normal starch (diet NS10), 10% waxy starch (diet WS10), 20% normal starch (diet NS20), 20% waxy starch (diet WS20) or no starch (control diet). Another diet was formulated with no carbohydrate, and contained 68% crude protein and 14% crude lipids (diet HP). Each experimental diet was fed to triplicate groups of 30 fish (initial weight: 23.3 g) on an equivalent feeding scheme for 12 weeks. The best growth performance and feed efficiency were achieved with fish fed the HP diet. Neither the level nor the nature of starch had measurable effects on growth performance of sea bass juveniles. Digestibility of starch was higher with waxy starch and decreased with increasing levels of starch in the diet. Whole-body composition and plasma metabolites, mainly glycemia, were not affected by the level and nature of the dietary starch. Data on enzyme activities suggest that dietary carbohydrates significantly improve protein utilization associated with increased glycolytic enzyme activities (GK and PK), as well as decreased gluconeogenic (FBPase) and amino acid catabolic (GDH) enzyme activities. The nature of dietary carbohydrates tested had little influence on performance criteria.
Comp Biochem Physiol A Mol Integr Physiol 2006 Jan
PMID:Effect of normal and waxy maize starch on growth, food utilization and hepatic glucose metabolism in European sea bass (Dicentrarchus labrax) juveniles. 1634 62

The compensatory changes of carbohydrate metabolism induced by fasting were investigated in frugivorous bats, Artibeus lituratus and Artibeus jamaicensis. For this purpose, plasma levels of glucose and lactate, liver and muscle glycogen content, rates of liver gluconeogenesis and the activity of related enzymes were determined in male bats. After a decrease during the first 48 h of fasting, plasma glucose levels remained constant until the end of the experimental period. Plasma lactate levels, extremely high in fed bats, decreased after 48 h of fasting. Similarly, liver glycogen content, markedly high in fed animals, was reduced to low levels after 24 h without food. Muscle glycogen was also reduced in fasted bats. The expected increase in liver gluconeogenesis during fasting was observed after 48 h of fasting. The activities of liver glucose-6-phosphatase and fructose-1,6-bisphosphatase were not affected by food withdrawn. On the other hand, fasting for 24 h induced an increase in the activity of liver cytosolic phosphoenolpyruvate carboxykinase. The data indicate that liver gluconeogenesis has an important role in the glucose homeostasis in frugivorous bats during prolonged periods of food deprivation. During short periods of fasting liver glycogenolysis seems to be the main responsible for the maintenance of glycemia.
Comp Biochem Physiol B Biochem Mol Biol 2006 Mar
PMID:Effect of fasting on carbohydrate metabolism in frugivorous bats (Artibeus lituratus and Artibeus jamaicensis). 1645 78

The role of rutin on carbohydrate metabolism in normal and streptozotocin (STZ)-induced diabetic rats was investigated in the present study. Administration of STZ led to a significant (p <0.05) increase in fasting plasma glucose and a decrease in insulin levels. The content of glycogen significantly (p <0.05) decreased in liver and muscle, but increased in kidney. The activity of hexokinase decreased whereas the activities of glucose-6-phosphatase and fructose-1,6-bisphosphatase significantly (p <0.05) increased in the tissues. Oral administration of rutin (100 mg/kg) to diabetic rats for a period of 45 days resulted in significant (p <0.05) alterations in the parameters studied but not in normal rats. A decrease of plasma glucose and increase in insulin levels were observed along with the restoration of glycogen content and the activities of carbohydrate metabolic enzymes in rutin-treated diabetic rats. The histopathological study of the pancreas revealed the protective role of rutin. There was an expansion of the islets and decreased fatty infiltrate of the islets in rutin-treated diabetic rats. In normal rats treated with rutin, we could not observe any significant change in all the parameters studied. Combined, these results show that rutin plays a positive role in carbohydrate metabolism and antioxidant status in diabetic rats.
J Biochem Mol Toxicol 2006
PMID:Rutin improves glucose homeostasis in streptozotocin diabetic tissues by altering glycolytic and gluconeogenic enzymes. 1661 78

Curative potential of riboflavin, niacin and ascorbic acid against tamoxifen mediated endometrial carcinoma was established by studies on carbohydrate metabolizing enzymes. The enzymes investigated were glycolytic enzymes namely, hexokinase; aldolase; phosphoglucoisomerase and the gluconeogenic enzymes namely, glucose-6-phosphatase and fructose-1, 6-biphosphatase in endometrial carcinoma bearing rats. A significant increase in glycolytic enzymes and a subsequent decrease in gluconeogenic enzymes were observed in plasma, liver and kidney of endometrial carcinoma animals. The administration of riboflavin (45 mg/kg bw/day), niacin (100 mg/kg bw/day) and ascorbic acid (200 mg/kg bw/day) along with tamoxifen (45 mg/kg bw/day) caused a significant decrease in the activity of glycolytic enzymes and a significant increase in the activities of gluconeogenic enzymes to near normal levels in experimental animals. Our results suggest that riboflavin, niacin and ascorbic acid have potential combination therapy against tamoxifen mediated secondary endometrial carcinoma in experimental rats. However, there were no deleterious side effects observed in combinants alone treated animals.
Mol Cell Biochem 2006 Aug
PMID:Therapeutic potential of riboflavin, niacin and ascorbic acid on carbohydrate metabolizing enzymes in secondary endometrial carcinoma bearing rats. 1669 16

The orphan receptor small heterodimer partner (SHP; NROB2) is a transcriptional repressor that inhibits nuclear receptor signaling in diverse metabolic pathways. Here, we report that SHP(-/-) mice exhibited hypoinsulinemia with age, which was associated with increased peripheral insulin sensitivity and increased response of isolated islets to glucose stimulation, yet maintain normal levels of blood glucose. Deficiency in SHP function resulted in up-regulation of glucose transporter 4 mRNA and glucose uptake in muscles, and overexpression of SHP in C2C12 cells inhibited both basal and peroxisomal proliferator-activated receptor gamma (PPARgamma) coactivator-1alpha-stimulated glucose transporter 4 expression and glucose uptake. SHP(-/-) hepatocytes showed markedly decreased basal glucose production in cultures, and SHP(-/-) livers had increased glycogen stores and were more sensitive to insulin inhibition of glucose output, which were concomitant with decreased expression for PPARgamma1, fatty acid translocase, glucose-6-phosphatase, and phosphoenol/pyruvate carboxykinase, and increased mRNAs for glucokinase and pyruvate kinase. In white fat, SHP deficiency resulted in up-regulation of genes involved in insulin sensitizing, including PPARgamma2 and adiponectin. We show that, at the transcriptional level, SHP directly represses adiponectin promoter activity by PPARgamma/liver receptor homolog-1. The results suggest that the increases in insulin sensitivity through multiple signaling pathways in muscle, liver, and fat, with an increase in islet secretory function, represent the complex mechanism whereby SHP deficiency leads to improvement in insulin sensitivity, secretion, and diabetes.
Mol Endocrinol 2006 Nov
PMID:Orphan receptor small heterodimer partner is an important mediator of glucose homeostasis. 1875 80

Insulin inhibits transcription of the genes encoding the glucose-6-phosphatase catalytic subunit (G6Pase), phosphoenolpyruvate carboxykinase, and IGF binding protein-1 through insulin response sequences (IRSs) that share the same core sequence, T(G/A)TTTT(G/T). The transcription factors FOXO1a and FOXO3a have been shown to bind these elements, but there are conflicting reports as to whether this binding correlates with the action of insulin on gene transcription. Some researchers concluded, from overexpression experiments using FOXO1a, that binding correlated with the insulin response, whereas others concluded, mainly from gel retardation competition experiments using FOXO3a, that it did not. We show here that, although these factors can differentially activate gene transcription in a context-dependent manner, these conflicting data are not explained by a difference in FOXO1a and FOXO3a binding specificity. Instead, we find that gel retardation competition and binding experiments give different results; the latter reveal a correlation between FOXO1a/3a binding and the inhibition of basal G6Pase gene transcription by insulin. In addition, these data show that the binding of FOXO1a/3a to two adjacent IRSs in the G6Pase promoter is cooperative and that promoter context alters the specific IRS base requirements for FOXO1a-stimulated fusion gene expression. Surprisingly, an analysis of insulin action mediated through the G6Pase and IGF binding protein-1 IRSs in the context of a heterologous thymidine kinase promoter reveals that signaling through the latter does not support the accepted model for insulin-stimulated FOXO nuclear exclusion.
Mol Endocrinol 2006 Nov
PMID:Correlation between FOXO1a (FKHR) and FOXO3a (FKHRL1) binding and the inhibition of basal glucose-6-phosphatase catalytic subunit gene transcription by insulin. 1684 May 35

The nutrient response mediated by feeding or fasting plays an important role in controlling gluconeogenic gene expression such as glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxylase (PEPCK). The FOXO family of forkhead transcription factor Foxo1 (mouse FOXO1) is a key regulator that stimulates the expression of gluconeogenic genes in the nucleus but is phosphorylated by Akt (also known as protein kinase B; PKB) and translocated to the cytoplasm in response to insulin. Although it has been widely accepted that the cellular signaling of insulin represses Foxo1 function through Akt-dependent phosphorylation, the molecular mechanism behind the modulation of Foxo1 function by nutrient responses, including feeding or fasting, remains unknown in vivo. We investigated the consequences of the nutritional changes in Akt-mediated Foxo1 phosphorylation and translocation in the liver using control C57BL/6 and diabetic db/db mice. We found that feeding promotes the phosphorylation and nuclear exclusion of Foxo1, whereas fasting counteracted them in C57BL/6 mice. Notably, db/db mice exhibited constitutive phosphorylation but dominant nuclear accumulation of Foxo1, even though CREB phosphorylation usually occurred in the fasted status. Furthermore, in contrast to C57BL/6 mice, the expression of G6Pase, PEPCK and PGC-1alpha genes during feeding was not down-regulated in db/db mice. Thus, we suggest that the accurate regulation of Foxo1 via Akt-dependent phosphorylation is required for physiological adaptation to different nutritional statuses.
Int J Mol Med 2006 Sep
PMID:Nutrient control of phosphorylation and translocation of Foxo1 in C57BL/6 and db/db mice. 1686 27

During liver development, hepatocytes undergo a maturation process that leads to the fully differentiated state. This relies at least in part on the coordinated action of liver-enriched transcription factors (LETFs), but little is known about the dynamics of this coordination. In this context we investigate here the role of the LETF hepatocyte nuclear factor 6 (HNF-6; also called Onecut-1) during hepatocyte differentiation. We show that HNF-6 knockout mouse fetuses have delayed expression of glucose-6-phosphatase (g6pc), which catalyzes the final step of gluconeogenesis and is a late marker of hepatocyte maturation. Using a combination of in vivo and in vitro gain- and loss-of-function approaches, we demonstrate that HNF-6 stimulates endogenous g6pc gene expression directly via a synergistic and interdependent action with HNF-4 and that it involves coordinate recruitment of the coactivator PGC-1alpha. The expression of HNF-6, HNF-4, and PGC-1alpha rises steadily during liver development and precedes that of g6pc. We provide evidence that threshold levels of HNF-6 are required to allow synergism between HNF-6, HNF-4, and PGC-1alpha to induce time-specific expression of g6pc. Our observations on the regulation of g6pc by HNF-6 provide a model whereby synergism, interdependency, and threshold concentrations of LETFs and coactivators determine time-specific expression of genes during liver development.
Mol Cell Biol 2006 Aug
PMID:Threshold levels of hepatocyte nuclear factor 6 (HNF-6) acting in synergy with HNF-4 and PGC-1alpha are required for time-specific gene expression during liver development. 1688 May 15


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