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PubMed1987

Effect of glipizide on hepatic fructose 2,6-bisphosphate concentration and glucose metabolism.

Glipizide raised, in a dose-dependent manner, the concentration of fructose 2,6-bisphosphate in hepatocytes isolated from 24-hour fasted rats and incubated in the presence of 10 mmol/L glucose. Simultaneously, the rate of L-lactate production, as well as the rate of 3H2O formation from (3-3H)glucose, increased markedly. The concentration of glipizide calculated as corresponding to the half-maximal effect in these metabolic parameters was 12 to 15 mumol/L. In hepatocytes isolated from fed rats, either normal or made diabetic by treatment with alloxan, glipizide inhibited the conversion of both (U-14C)pyruvate and (U-14C)lactate to (14C)glucose; an inverse correlation was established between hepatocyte fructose 2,6-bisphosphate levels and the rate of gluconeogenesis. The increase of fructose 2,6-bisphosphate concentration elicited by glipizide, which occurs without a significant modification of either 6-phospho-fructo 2-kinase activity or hepatocyte cyclic AMP levels, seems to be related to a significant accumulation of hexose 6-phosphates (glucose 6-phosphate and fructose 6-phosphate) in the hepatic cells.

Animals↗
PubMed1984

State of sulfhydryl in selenite cataract.

A dose of 20 mumol selenite/kg body weight is a potent and a very rapid inducer of cataracts in young rats. We investigated the rate at which physiological concentrations of selenite would catalyze the oxidation of glutathione in vitro and found that selenite was a strong sulfhydryl oxidant. To test if selenite had the same effect in vivo, the oxidation state of five kinds of lenticular sulfur were measured in suckling rats following a cataractous dose of selenite. The measurements included reduced glutathione (GSH), oxidized glutathione (GSSG), protein-bound glutathione ( PSSG ), reduced protein sulfhydryl ( PSH ), and oxidized protein sulfhydryl ( PSSP ). While selenite caused a 44% decrease in lens GSH by 6 days postinjection, there was no concurrent increase in either GSSG or PSSG . Likewise, there was no evidence for increased oxidation of PSH to PSSP . To determine if GSH loss were the cause of the selenite cataracts, we injected normal rats with the glutathione synthesis inhibitor buthionine sulfoximine (BSO). Lens GSH dropped more than 96% by 4 days post-BSO injection; however, no cataracts formed. Thus, selenite cataract does not appear to be caused by extensive sulfhydryl oxidation and cannot be attributed exclusively to GSH loss.

Animals↗
PubMed1992

The regulatory protein of liver glucokinase.

Fructose, sorbitol and D-glyceraldehyde stimulate the rate of glucose phosphorylation in isolated hepatocytes. This effect is mediated by fructose 1-phosphate, which releases the inhibition exerted by a regulatory protein on liver glucokinase. In the presence of fructose 6-phosphate, the regulatory protein binds to, and inhibits, liver glucokinase. Fructose 1-phosphate antagonizes this inhibition by causing dissociation of the glucokinase-regulatory protein complex. Both phosphate esters act by binding to the regulatory protein, and by presumably causing changes in its conformation. The regulatory protein behaves as a fully competitive inhibitor. It inhibits liver glucokinase from various species, and rat islet glucokinase, but has no effect on hexokinases from mammalian tissues or from yeast, or on glucokinase from microorganisms. Kinetic studies indicate that the regulatory protein binds to glucokinase at a site distinct from the catalytic site. Several phosphate esters, mainly polyol-phosphates, were found to mimick the effect of fructose 6-phosphate. The most potent is sorbitol 6-phosphate, suggesting that fructose 6-phosphate is recognized by the regulatory protein in its open-chain configuration. Other phosphate esters and Pi have a fructose 1-phosphate-like effect. The stimulatory effect of fructose on glucose phosphorylation is observed not only in isolated hepatocytes but also in the livers of anesthetized rats. This suggests that fructose could be a nutritional signal causing an increase in the hepatic glucose uptake.

Allosteric Regulation↗
PubMed1972

ATP formation.

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Adenosine Diphosphate↗