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PubMed1983

Reciprocal regulation of fructose 1,6-bisphosphatase and phosphofructokinase by fructose 2,6-bisphosphate in swine kidney.

The effect of fructose 2,6-P2, AMP and substrates on the coordinate inhibition of FBPase and activation of PFK in swine kidney has been examined. Fructose 2,6-P2 inhibits the activity of FBPase and stimulates the activity of PFK in the presence of inhibitory concentrations of ATP. Under similar conditions 2.2 microM fructose 2,6-P2 was required for 50% inhibition of FBPase and 0.04 microM fructose 2,6-P2 restored 50% of the activity of PFK. Fructose 2,6-P2 also enhanced the allosteric activation of PFK by AMP and it increased the extent of inhibition of FBPase by AMP. Fructose 2,6-P2, AMP and fructose 6-P act cooperatively to stimulate the activity of PFK whereas the same latter two effectors and fructose 1,6-P2 inhibit the activity of FBPase. Taken collectively, these results suggest that an increase in the intracellular level of fructose 2,6-P2 during gluconeogenesis could effectively overcome the inhibition of PFK by ATP and simultaneously inactivate FBPase. When the level of fructose 2,6-P2 is low, a glycolytic state would be restored, since under these conditions PFK would be inhibited by ATP and FBPase would be active.

Adenosine Monophosphate↗
PubMed1983

Glutamine synthetase and fructose-1, 6-diphosphatase activity in the putamen of control and Huntington's disease brain post mortem.

There is a linear negative correlation between the activities of glutamine synthetase and fructose-1, 6-diphosphatase in normal Human putamen autopsy samples, and also in the Huntington's disease putamen. However, glutamine synthetase activity is reduced in choreic brain samples, while fructose-1, 6-diphosphatase activity is normal. The ratio of fructose-1, 6-diphosphatase to glutamine synthetase is therefore increased in Huntington's disease. The products of the two reactions, glutamine and fructose-6-phosphate, are the starting substrates for glycolipid and glycoprotein biosynthesis, via the glutamine:fructose-6-phosphate aminotransferase catalysed formation of glucoseamine-6-phosphate. The alternative metabolic route of fructose-6-phosphate leads to glycogen. The availability of glutamine, and the activity of glutamine synthetase may control fructose-6-phosphate metabolism, and the increased ratio of fructose-1,6-diphosphatase to glutamine synthetase in Huntington's disease may explain the accumulation of glycogen, and the reduction in ganglioside levels reported in this state.

Fructose-Bisphosphatase↗
PubMed1990

The role of acetate in alcohol-induced alterations of uterine glucose metabolism in the mouse during pregnancy.

The acute exposure of mice to ethanol during post-implantation pregnancy has been reported to cause alterations in the levels of several glycolytic intermediates in the uterus, suggesting a possible indirect mechanism of alcohol embryo-toxicity. The present study was undertaken to assess whether the ethanol metabolite, acetate is implicated in this phenomenon. Blood and uterine alcohol concentrations in day 9--pregnant Quackenbush Swiss mice were maximal 15 minutes after the intraperitoneal injection of ethanol (3.5 g/kg body weight), and fell to almost negligible levels 6 hours later. In response to this treatment, the levels of blood and uterine acetate increased, liver glycogen decreased, plasma glucose increased, and uterine glucose, glucose-6-phosphate (G-6-P), fructose-6-phosphate (F-6-P), and citrate increased. When acetate was administered to pregnant mice in amounts approximating those generated by exposure to alcohol, the levels of uterine F-6-P and citrate increased while other metabolic parameters remained unaffected. The administration of 4-methylpyrazole to mice subsequently treated with alcohol produced conditions of alcohol exposure in the absence of ethanol-derived acetate and depressed the ethanol-induced rise in uterine G-6-P and citrate. The results support the notion that acetate contributes to the alcohol-induced alterations in metabolism, at least as far as the regulation of uterine citrate and hexose monophosphates are concerned. This, together with stress responses induced by exposure to the acute dose of alcohol, may present mechanisms underlying the fetal alcohol syndrome associated in particular with "binge" drinking.

Acetates↗
PubMed1995

Effects of an aldose reductase inhibitor on erythrocyte fructose 3-phosphate and sorbitol 3-phosphate levels in diabetic patients.

Fructose 3-phosphate and sorbitol 3-phosphate are novel metabolites that have been shown to associate with the polyol pathway in animal experiments. Fructose 3-phosphate is of particular interest because of its potent glycation capability as compared with other glycolytic intermediates, e.g., fructose. We observed the effects of treatment with epalrestat, an aldose reductase inhibitor, on their concentrations in erythrocytes from diabetic patients. The levels of both metabolites were significantly higher in diabetic patients than in non-diabetic subjects. A group of patients who had been treated with epalrestat showed significantly lower levels of both metabolites as compared with those untreated. A treatment of three patients with epalrestat for one month resulted in obvious decreases in their concentrations. The results suggest a possible explanation for the preventive effect of an aldose reductase inhibitor on nonenzymatic glycation.

Adult↗
PubMed1982

Adverse effects of fructose in perfused livers of diabetic rats.

Livers isolated from both fed normal and alloxan diabetic rats were perfused for 30 min using Krebs-Henseleit bicarbonate blood buffer medium followed by 10 min flow-through infusions with either 5 mM or 28 mM fructose concentrations. In livers of normal and diabetic rats, both 5 mM and 28 mM fructose concentrations produced an elevation in tissue cyclic AMP levels, activation of glycogen phosphorylase, increased protein kinase activity, decreased tissue ATP levels, large increases in tissue fructose-1-phosphate, and variable effects upon glycogen synthase. These results are consistent with previously reported cyclic AMP mediated activation of glycogen phosphorylase by fructose via protein kinase in normal rat liver. In addition, both 5 mM and 28 mM fructose infusion resulted in large decreases in normal and diabetic synthase phosphatase activity. Therefore, these results in both normal and diabetic livers are inconsistent with a direct beneficial effect of fructose in the isolated perfused rat liver.

Adenosine Triphosphate↗
PubMed1993

Measuring glucose and fructose-6-phosphate cycling in liver in vivo.

Approaches measuring futile cycling of glucose and fructose-6-phosphate (fructose-6-P) in liver in vivo depend on assumptions about the fates of hydrogens bound to specific carbons of glucose. Thus, 3H of [2-3H]glucose has been assumed to be completely removed after its conversion to glucose-6-P, [3-3H]glucose after its conversion to fructose-1,6-bisP, and [6-3H]glucose not at all. Previous measurements have shown that these assumptions are incompletely fulfilled. Corrections to estimates of cycling can be made when detritiations of [2-3H]glucose and [3-3H]glucose are not complete, and detritiation of [6-3H]glucose occurs. How the corrections can be made is presented using data previously reported on giving labeled glucoses to humans after an overnight fast and on infusing a glucose load. Estimates of glucose cycling nearly double, and that of fructose-6-P cycling almost triples. Estimates of hepatic glucose production as measured with [6-3H]glucose decrease. Correction of estimates of cycling under other conditions may very well be similarly affected. Thus, rates of glucose and fructose-6-P cycling appear to be substantially more than previously estimated. Quantitation under a given condition requires measurements to be made of the extent to which assumptions as to the fate of labeled hydrogen of the glucoses are fulfilled. The uncertain extent of exchange of label catalyzed by transaldolase and detritiation in the pentose cycle, the failure of fructose-6-P cycling to be expressed through detritiation of 3H from [3-3H]glucose, and possible isotope effects still limit the confidence that can be placed in such estimates.

Fructosephosphates↗
PubMed1995

Identification of galactitol 2-phosphate and galactitol 3-phosphate in the lens of galactose-fed rats.

Production of unusual phosphorylated metabolites in the lens is one of several changes caused by hyperglycemia. Sorbitol 3-phosphate (Sor-3P) and fructose 3-phosphate (Fru-3P) are two such compounds identified in the diabetic lens, and galactitol 2-phosphate (Gal-2P) and galactitol 3-phosphate (Gal-3P) are identified here in the galactosemic lens. These new compounds are the first example of galactitol metabolism in mammalian tissue other than liver. Sor-3P and Fru-3P are also present in the galactosemic lens, apparently synthesized directly from their precursors, sorbitol and fructose, which are elevated in the lens due to increased flux of glucose through the aldose reductase (AR) pathway. The NADPH necessary to support this increased flux is derived from activation of the hexose monophosphate shunt (HMPS), which is clearly demonstrated by a large increase in the concentration of sedoheptulose 7-phosphate (Sed-7P), a HMPS-specific metabolite. Additionally, during 3 weeks of galactose feeding, there is a dramatic increase in lenticular concentrations of galactitol, sorbitol, galactose, and fructose and a sharp decrease in inositol. Glucose remains unchanged. A precipitous loss of both phosphorylated and nonphosphorylated metabolites occurs after 3 weeks, possibly due to lens rupture.

Animals↗