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PubMed1968

Stimulation of pentose phosphate pathway dehydrogenase enzyme activities in ethionine-treated mice.

1. Mice treated with ethionine (intraperitoneally, 5mg./day for 4 days or 10mg./day for 3 days) showed a profound loss of hepatic glycogen, a decrease of glycogen synthetase activity, a development of hypoglycaemia, a two- to five-fold increase in the activity of glucose 6-phosphate dehydrogenase but no change in 6-phosphogluconate dehydrogenase and an earlier manifestation of the solubilization of phosphorylase as compared with glycogen synthetase. The administration of ATP did not prevent these effects. 2. During the early post-injection period (2-3 days) there was a further enhancement of the activity of glucose 6-phosphate dehydrogenase (tenfold) in the liver and a clear elevation of 6-phosphogluconate dehydrogenase activity (twofold). Subsequently, the glycogen concentration was restored, followed by an earlier reassociation of glycogen particle with phosphorylase than with glycogen synthetase, along with a disappearance of ethionine effect at about the eighteenth day. 3. Glucose 6-phosphate dehydrogenase from both control and ethionine-treated animals showed a marked preference for glucose 6-phosphate as substrate rather than for galactose 6-phosphate, whose rate of oxidation was only 10% of that of the glucose 6-phosphate. 4. Since actinomycin D, puromycin, 5-fluorouracil and dl-p-fluorophenylalanine failed to block the ethionine-enhanced glucose 6-phosphate dehydrogenase activity, the possibility that new enzyme protein synthesis is responsible for the effect is doubtful.

Adenosine Triphosphate↗
PubMed1988

Repression of pentose phosphate pathway dehydrogenase synthesis and mRNA by dietary fat in rats.

We have studied the effects of polyunsaturated fatty acid and its metabolism on the activity, relative synthesis and mRNA levels for rat hepatic glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD). Rats were meal-fed high carbohydrate diets containing either no fat, 5% safflower oil or 5% safflower oil + eicosa-5,8,11,14-tetraynoic acid (TYA). Hepatocytes were isolated and used as a source of RNA, de novo radiolabeled protein and postmitochondrial supernatant for enzyme assay. Dietary safflower oil, as a source of linoleic acid, repressed G6PD activity, synthesis and mRNA levels two- to threefold without significantly changing the amount of carbohydrate consumed. Similar but smaller changes were observed for 6PGD. Dietary fat + TYA (an analogue of arachidonate that inhibits normal metabolism of linoleic acid) prevented the fat-dependent lowering of G6PD and 6PGD activity, synthesis and mRNA levels. Our results suggest that a metabolite of linoleic acid regulates the activity of two lipogenic enzymes, G6PD and 6PGD, by lowering gene expression or mRNA processing or stability.

5,8,11,14-Eicosatetraynoic Acid↗