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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)

Potassium chloride concentrations of 100-150 mM were shown to inhibit (20-40%) human and rat liver microsomal glucose-6-phosphatase when the substrate was reduced to physiological concentration. When the enzyme was solubilized by treatment of microsomes with A12O3 the inhibition could be observed at greater substrate concentrations. Since potassium deprivation is associated with hyperglycemia in both animals and man, these observations may have physiological significance.
Acta Diabetol Lat
PMID:Effect of potassium on human and rat liver glucose-6-phosphatase. 19 67

Colenol, a diterpenoid isolated from the roots of Coleus forskohlii stimulates the release of insulin and glucagon from the islets both in vitro and in vivo. Colenol-stimulated release of glucagon from islets in vitro is much more pronounced as compared to that of insulin. Glucose concentration of 5.6 mM in the medium is required for the colenol stimulation of insulin release. Feeding of coleonol to alloxan diabetic rats cause 36.5% increase in blood glucose level as compared to alloxan diabetic control. Oral feeding of coleonol for 7 days to normal rats causes increase in blood glucose, serum insulin, glucagon and free fatty acid levels with corresponding increase in glucose-6-phosphatase activity and depletion of liver glycogen. Predominant stimulation of A-cells by coleonol is suggested for the above effects.
Acta Diabetol Lat
PMID:Insulin and glucagon releasing activity of coleonol (forskolin) and its effect on blood glucose level in normal and alloxan diabetic rats. 165 May 16

Substrate cycles (SC) are formed by a 'forward pathway' (FP) and a 'backward pathway' (BP), the difference between FP and BP forming the 'metabolic flux' (MF) through the route of which the cycle is part. SC modulate regulatory effects, i.e. amplify or reduce the % change in MF compared to the % change in FP and BP, thus affecting the sensitivity to regulatory factors, including hormones. A formula is given to calculate (with an approximation of +/- 0.5) the 'flux response index' (FRI), i.e. the factor by which the % change in FP plus the % change in BP must be multiplied to obtain the % change in metabolic flux, when FP and BP undergo opposite, non-unidirectional changes (as is often the case in metabolic regulation). The formula is: FRI = [( FP + BP)/(FP-BP)]/2. By this formula we evaluated the hepatic activities of glucose-6-phosphatase and glucokinase (which roughly reflect hepatic glucose production and uptake, respectively), i.e. the two enzymes that catalyze the cycle between glucose-6-phosphate (glucose-6-P) and glucose. Based on data obtained in normal, nonobese diabetic and obese diabetic subjects as well as in normal, streptozotocin-diabetic, and obese diabetic (ob/ob) mice, we found that FRI was reduced in non-obese diabetic humans and animals whereas it was increased in obese-diabetic humans and mice, compared to normal controls. Thus, diabetes without obesity decreases, and obesity with diabetes increases, the sensitivity of the glucose-6-P/glucose cycle to regulatory agents.
Acta Diabetol Lat
PMID:A formula for quantifying the effects of substrate cycles (futile cycles) on metabolic regulation. Its application to glucose futile cycle in liver as studied by glucose-6-phosphatase/glucokinase determinations. 215 82

Kinetic studies of the histochemical and histoenzymatic behavior of rabbit pancreatic parenchymas were performed 5, 30 and 90 days after Wirsung duct ligation. In control pancreas, some enzyme activities (EA) were more prominent in Langerhans islets [glucose-6-phosphatase, glucose-6-phosphate dehydrogenase (DH), isocitrate DH, glycerol-3-phosphate DH, NADPH DH], others were strongly marked in acini and ducts (alkaline phosphatase, beta-glucuronidase, acid esterase aryl-sulfatase). Histochemical and enzyme abnormalities observed in experimental rabbits reflect the post-ligation degenerative and reactive processes in both exocrine and endocrine pancreas: (1) the decrease in Krebs cycle and pentose pathway linked EA and the increased lysosomal and acid phosphatase EA reflect early (day 5) degeneration and necrosis of islets and acini (day 30); (2) proliferative processes in developed ductal epithelia are shown by an increase in both glycolytic and lysosomal EA (days 30 and 90); (3) connective tissue neogenesis and interstitial fibrosis occurred as shown by activated beta-glucuronidase, aryl-sulfatase, alkaline phosphatase and increased ribonucleoproteins and glycoaminoglycans contents (day 30); (4) on day 90, the neoformed cell clusters presenting glucose-6-phosphatase positivity (B-cell marker) are seen in the pancreas remnant. At the same time, blood insulin level increases correlated with a decrease of hyperglycemia.
Acta Diabetol Lat
PMID:Cell features in pancreas of prediabetic and diabetic rabbits after Wirsung duct ligation. Histochemical and histoenzymatic studies. 233 24

Tolbutamide and carbutamide given orally to fasted rats cause a rise in the liver glycogen content 1(1/2) to 3(1/2) hr. after administration of the drugs. Glycogen accumulates preferentially in the right lobe. Subcutaneously injected tolbutamide has the same effect. Both sulphonylureas cause inhibition of glucose-6-phosphatase activity of rat liver homogenates in vitro, but at drug concentrations comparable with those found in plasma of treated patients the degree of inhibition is less than 10%. Livers from treated rats show normal glucose-6-phosphatase activity. The glucose uptake of the isolated rat diaphragm is unaffected by the sulphonylureas added in vitro. Diaphragms from treated rats show normal glucose uptake in the presence or absence of insulin. The inferences to be drawn from these results are discussed in the light of previous work. It is concluded that the sulphonylureas exert hypoglycaemic action by inhibiting glycogenolysis and it is suggested that they might do so by inhibiting release of glucagon from the pancreas.
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PMID:The action of hypoglycaemic sulphonylureas on carbohydrate metabolism in the fasted rat. 1346 Feb 43

Muscle tissue has been considered to be a major regulator of systemic glucose homeostasis. Glucose normally provides energy sources for tissues of the body. Its uptake by muscle requires a secretion of insulin. The initial step of glucose utilization requires the transport of glucose into the cells. The insulin-receptor complex stimulates the cellular uptake of glucose. In the well-fed state muscle contains about 1% of its weight as glycogen. Because of its mass, muscle contains almost four times as much glycogen as the liver. Muscle glycogen is not directly available as a source of blood glucose because muscle lacks glucose-6-phosphatase. During muscular activity, glycogen is converted to lactate and then into blood glucose in the liver.
Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw 2003
PMID:[The role of skeletal muscle in the regulation of glucose homeostasis]. 1457 19