Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P36959 (guanosine monophosphate reductase)
 36 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in vivo effect of dehydroepiandrosterone (DHEA) on hepatic glycogen content and on glucose metabolizing enzymes was investigated in male and female Sprague-Dawley rats treated with 0.6% (w/w) DHEA in the diet for 3, 7, 14, 28 and 140 days. The glycolytic enzymes studied (glucokinase, hexokinase, pyruvate kinase) showed a significant persistent decrease in activity in both sexes after 3-7 days of treatment. Gluconeogenic enzymes (glucose-6-phosphatase, fructose-1,6-bisphosphatase) were increased after 3 days, but decreased after 7-14 days. Glycolytic enzymes showed a stronger reduction than gluconeogenic enzymes. Females were slightly more affected than males. Glucose-6-phosphate dehydrogenase was unchanged in females, but increased in males. Glycogen content and the activity of glycogen phosphorylase were reduced after 3 days of treatment. mRNA analysis of glucokinase and phosphorylase indicated that these enzyme alterations were accompanied by reduced transcriptional expression, while glucose-6-phosphate dehydrogenase mRNA levels were unchanged. Withdrawal of DHEA from 4 week-treated rats was associated with an almost complete reversibility of the enzyme alterations after 2 weeks. After long-term treatment (140 days) glucokinase, glucose-6-phosphatase and fructose-1,6-bisphosphatase activities were no longer altered. Since DHEA treatment affects the key enzymes of glucose metabolic pathways in the same sense, it is suggested that DHEA does not regulate individual enzymes but rather common regulatory factors or signalling pathways.
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PMID:Dehydroepiandrosterone reduces expression of glycolytic and gluconeogenic enzymes in the liver of male and female rats. 2154 66

A 13-week feeding trial was carried out with juvenile rainbow trout to test two diets: a control diet without astaxanthin (AX) supplementation (CTRL diet), and a diet supplemented with 100 mg/kg of synthetic AX (ASTA diet). During the last week of the feeding trial, fish were exposed to episodic hyperoxia challenge for 8 consecutive hours per day. Episodic hyperoxia induced physiological stress responses characterized by a significant increase in plasma cortisol and hepatic glycogen and a decrease in plasma glucose levels. The decrease of plasma glucose and the increase of hepatic glycogen content due to episodic hyperoxia were emphasized with the ASTA diet. Hyperoxia led to an increase in thiobarbituric acid-reactive substances in the muscle, diminished by dietary AX supplementation in both liver and muscle. Muscle and liver AX were increased and decreased respectively after 7-day episodic hyperoxia, leading to an increase in flesh redness. This augment of muscle AX could not be attributed to AX mobilization, since plasma AX was not affected by hyperoxia. Moreover, hyperoxia decreased most of antioxidant enzyme activities in liver, whereas dietary AX supplementation specifically increased glutathione reductase activity. A higher mRNA level of hepatic glutathione reductase, thioredoxin reductase, and glutamate-cysteine ligase in trout fed the ASTA diet suggests the role of AX in glutathione and thioredoxin recycling and in de novo glutathione synthesis. Indeed, dietary AX supplementation improved the ratio between reduced and oxidized glutathione (GSH/GSSG) in liver. In addition, the ASTA diet up-regulated glucokinase and glucose-6-phosphate dehydrogenase mRNA level in the liver, signaling that dietary AX supplementation may also stimulate the oxidative phase of the pentose phosphate pathway that produces NADPH, which provides reducing power that counteracts oxidative stress. The present results provide a broader understanding of the mechanisms by which dietary AX is involved in the reduction of oxidative status.
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PMID:Influence of Dietary Astaxanthin on the Hepatic Oxidative Stress Response Caused by Episodic Hyperoxia in Rainbow Trout. 3181 93