Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rat liver glucose 6-phosphate dehydrogenase (G6PD) and malic enzyme (ME) activities were increased by starvation-refeeding to levels above those found in rats fed ad libitum. The increases in enzyme activities above ad libitum-fed levels were prevented by 8-azaguanine and 6-azauridine, but not by 2-azauridine. Blood insulin levels were not affected at the time studied. Two aza analogs, 8-azaadenine and 5-azacytidine, proved to be too toxic in this type of studies. Since 8-azahypoxanthine, 8-azaxanthine and 5-azauracil were neither effective in preventing the enzyme overshoot, nor toxic to the animals, it was concluded that the toxiciyty to the animals of 8-azaadenine and 5-azacytidine is due to the compounds themselves rather than to the breakdown products.
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PMID:Effect of aza-substituted nucleotides on the starve-refeed response of rats. 4 59

The role of dietary unsaturated fat in the control of hepatic glucose-6-phosphate dehydrogenase (G6PD) (EC 1.1.1.49) and malic enzyme (ME) (EC 1.1.1.40) was studied in rats subjected to one or two cycles of starvation-refeeding. Rats starved and refed a control (5% corn oil) diet showed a threefold increase in G6PD activity and a twofold increase in ME activity compared to ad libitum-fed rats. After a second cycle of starvation-refeeding G6PD and ME activities showed fourfold and threefold increases, respectively, as compared to ad libitum-fed rats. Feeding rats diets containing 8% linoleic acid (as triglycerides) prevented the increase in G6PD and ME activities upon starvation-refeeding, diets with oleic, palmitic, and stearic acis when fed did not prevent this increase. Feeding rats various combinations of linoleic, linolenic and oleic acids following starvation prevented the additional increase in G6PD and ME activities after a second starvation-refeeding cycle; however, linoleic acid fed alone during the first refeeding prevented the additional increase in ME activity but not in G6PD activity. It is suggested that the dietary control of these enzymes involves one or more specific polyunsaturated fatty acids.
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PMID:Dietary fatty acids on the control of glucose-6-phosphate dehydrogenase and malic enzyme in the starved-refed rat. 12 45

The responses of glucose-6-phosphate dehydrogenase (G6PD) (EC 1.1.1.49) and malic enzyme (ME) (EC 1.1.1.40) were studied in liver and adipose tissue of rats fed for 2 days a high glucose diet containing levels of synthetic trilinolein ranging from 0 to 25% (w/w) of the diet (trilinolein was substituted for glucose). One group of rats was starved for 2 days before the trilinolein-containing diets were fed (starved-refed); a second group of rats was fed a fat-free diet for 7 days before the trilinolein-containing diets were fed (ad libitum). Liver G6PD activity decreased exponentially and liver ME activity decreased linearly with increasing dietary trilinolein in starved-refed rats, but did not decrease significantly in ad libitum fed rats. Total liver lipid decreased exponentially with increasing trilinolein in starved-refed rats, but increased exponentially in ad libitum fed rats. Adipose tissue G6PD and ME activities decreased slightly with increasing trilinolein in starved-refed rats, but did not decrease in ad libitum fed rats. When the data were adjusted by analysis of covariance for differences in glucose intake, the liver responses in starved-refed rats were still significant but the adipose tissue responses were not, indicating that the responses of adipose tissue (but not of liver) may have resulted from decreased glucose intake rather than from increased trilinolein intake. The results suggest that dietary trilinolein inhibits the characteristic increase in liver G6PD, ME and total lipids upon starvation-refeeding. However, after the levels of these parameters have been increased by feeding a fat-free diet they cannot be decreased by dietary trilinolein in 2 days.
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PMID:Regulation of glucose-6-phosphate dehydrogenase and malic enzyme in liver and adipose tissue: effect of dietary trilinolein level in starved-refed and ad libitum-fed rats. 44 48

Activity of dehydrogenases related to pentosephosphate pathway was not distinctly altered in soluble fraction of kidney cortex and medulla after 48 and 72 hrs of starvation. In diabetes the activity of these enzymes in rat kidney, as distinct from liver tissue, was not decreased but it was elevated and within 72 hrs after administration of alloxan the activity of glucose-6-phosphate dehydrogenase was increased 2-fold and the activity of 6-phosphogluconate dehydrogenase was increased by 30% above the normal level. Content of free fatty acids was also increased in kidney cortex of diabetic rats within 72 hrs after administration of alloxan. Alterations in content of free fatty acids were not observed either in kidney of diabetic animals within other studied periods (6 and 14-16 days) of treatment or in the tissue of starved rats. The data obtained suggest that free fatty acids do not participate immediately in controlling effect on dehydrogenases of pentosephosphate pathway in kidney in vivo.
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PMID:[Effect of starvation and diabetes on the activity of glucose-6-phosphate and 6-phosphogluconate dehydrogenases and on the free fatty acid content of rat kidney cortex and medulla]. 66 69

When islets from mice were incubated with 16.7 mM-glucose, previous starvation for 48 h decreased the rate of insulin release by approx. 50% and glucose utilization was decreased by approx. 35%. The maximally extractable activity of glucose 6-phosphate dehydrogenase was diminished by 28% after starvation. The formation of 14CO2 from both [1-14C]glucose was, however, higher than the rate of oxidation of [6-14C]-glucose in islets from both fed and starved mice. The fraction of glucose utilized that was oxidized (specific 14CO2 yield) ranged from one-fifth to one-third and was higher in islets from starved mice with both [1-14C]glucose and [6-14C]glucose as substrate. The contribution of pentose-cycle oxidation to total glucose metabolism was small (3% in the fed state and 4% in the starved state). The absolute rates of glucose carbon metabolism via the pentose-cycle oxidation to total glucose metabolism was small (3% in the fed state and 4% in the starved state). The absolute rates of glucose carbon metabolism via the pentose cycle and the turnover of NADPH in this pathway were identical in islets from fed and starved animals. After incubation at 16.7 mM-glucose for 30 min the contents of glucose (6-phosphate and 6-phosphogluconate were both unchanged by starvation. It is concluded that there is no correlation between the decreased sensitivity of the insulin secretory mechanism during starvation and the metabolism of glucose via the pentose cycle, the islet content of glucose 6-phosphate or 6-phosphogluconate.
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PMID:The pentose cycle and insulin release in isolated mouse pancreatic islets during starvation. 77 71

These studies were undertaken to determine the mechanism by which intravenously administered lead salts inhibit hepatic gluconeogenesis. Within 1 h after the intravenous administration of lead acetate (10 mg), there is 97% inhibition of CO2 fixation in isolated rat liver mitochondria. This effect is concentration-dependent. The induction of phosphoenolpyruvate carboxykinase activity observed with starvation was also inhibited by intravenously administered lead acetate, but the activities of pyruvate kinase, glucose 6-phosphate dehydrogenase and pyruvate carboxylase were unaffected, as was the oxidation of palmitate and palmitoyl-CoA by mitochondria from Pb2+-treated animals. The addition of reduced glutathione to mitochondria from Pb2+-treated animals had no effect on the inhibited CO2 fixation. ATP concentrations in mitochondria from Pb2+-treated animals are decreased and the dose-response relationships for the effect of Pb2+ on CO2 fixation and ATP concentrations correspond. We conclude that the decrease in mitochondrial ATP in Pb2+-treated animals is probably responsible for the marked inhibition ov CO2 fixation, and hence the impairment of gluconeogenesis from alanine, lactate and pyruvate observed by others.
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PMID:Inhibition of carbon dioxide fixation by lead acetate in rat liver mitochondria. 90 20

The responses of liver glycogen and glucose-6-phosphate dehydrogenase (G6PD) (EC 1.1.1.49) to a high glucose, adequate protein diet were compared between rats previously starved 2 days, then refed a high protein, carbohydrate-free diet for 2 days, and rats previously fed the high protein diet for 4 days. Glycogen levels increased dramatically during the first day the high carbohydrate diet was fed, then decreased gradually on the second day. The response was the same regardless of whether the rats had been starved more before the high protein diet was fed. Liver G6PD activity also increased when the high carbohydrate diet was fed, and continued to increase on the second day. The increase in G6PD, however, was significantly greater in the rats which had been starved before the high protein diet was fed. It is suggested that some process occurs during starvation that predisposes the induction of G6PD upon refeeding a high carbohydrate diet, over and above any effect of glycogen accumulation and breakdown. Glucose or glucose-6-phosphate derived from glycogen does not appear to be the primary inducer of G6PD in rat liver.
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PMID:Independence of glycogen accumulation and glucose-6-phosphate dehydrogenase induction in rat liver. 92 58

The importance of the adrenal hormones in the lipogenic responses to meal-feeding or starvation-refeeding was studied. In experiment 1, intact or adrenalectomized (ADX) rats were either ad libitum-fed or meal-fed a 65% glucose diet for 21 days or until moribund (ADX rats only). Serum glucose and electrolytes (Ca++, Mg++, Na+, K+), hepatic glycogen and glucose-6-phosphate dehydrogenase (G6PD) and malic enzyme (ME) were determined. ADX rats died within 10 days after the initiation of meal-feeding and were hypoglycemic with low liver glycogen levels and low enzyme activities. No differences in serum electrolytes were observed. In the second experiment, ADX and intact rats of varying initial weights were weight paired and meal-fed. When the ADX rat died, his intact control was killed and both carcasses assayed for fat content. Heavier rats with presumably more carcass fat survived meal-feeding longer than the lighter rats. Rats died when they had lost all but 2 to 3 g carcass lipid. In experiments 3 and 4, ADX and intact rats were subjected to starvation-refeeding. In experiment 4, additional ADX groups were given supplemental doses of cortisol (0.75 mg/kg, subcutaneous, 2 times daily) during either the starvation period, the refeeding period or during both periods. The activities of hepatic G6PD and ME were determined as well as the levels of liver lipid in experiment 4. Intact starved-refed rats had the usual enzyme overshoot, whereas ADX starved-refed rats did not. Cortisol-treated ADX starved-refed rats had as great an enzyme overshoot as the intact rats and as great an increase in liver lipid. These results suggest that ADX rats die when meal-fed the glucose diet, because they are unable to store sufficient metabolic fuel for use during the starvation phase of the meal-feeding cycle. Further, the results show that glucocorticoids are required for the induction of de novo enzyme synthesis.
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PMID:Further studies on the role of the adrenal hormones in responses of rats to meal-feeding. 99 59

Meal-feeding of a high sucrose diet produces a diurnal cycle (i.e., food response) in glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD) levels resulting in an elevated level of these enzymes at approximately 12 hours after the start of a 2-hour meal and a return to base level by 24 hours. The effects of actinomycin D and cycloheximide on the 12-hour increases in G6PD and 6GPD were determined. Cycloheximide completely blocked the increase in G6PD if administered 2 or 4 hours after start of the meal, while actinomycin D completely blocked the increase in G6PD if administered at 2 hours and almost completely at 4 hours after start of the meal. These results were obtained previously with starved rats refed a sucrose diet. The diurnal increases in G6PD and 6PGD in meal-fed rats and the induction of G6PD in starved-refed rats thus appear to be regulated by the same mechanism requires RNA synthesis within 4 hours after start of re-feeding. The response of 6PGD to cycloheximide and to actinomycin D at 2 or 4 hours after start of the meal is essentially the same as that of G6PD. These data suggest that the increases in G6PD and 6PGD (and other enzymes) brought about by carbohydrate refeeding AFTER starvation or by carbohydrate meal-feeding on a diurnal cycle are mediated by a rapid change in RNA synthesis. This appears most compatible with a coordinate control of gene expression through messenger RNA synthesis.
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PMID:Regulation of glucose-6 phosphate dehydrogenase and 6-phosphogluconate dehydrogenase in the meal-fed rat. 117 Feb 87

The effect of a high fructose diet on lipogenesis was studied in rats. Male and female rats were divided into three groups and were fed a high carbohydrate diet ad libitum for 4 days: group 1 was fed a high cornstarch diet, group 2 was fed a high fructose diet without starvation, and group 3 was fed a high fructose diet after 2 days of starvation. The activities of lipogenic enzymes, i.e., glucose-6-phosphate dehydrogenase and malic enzyme were assayed in liver, adipose tissue, and small intestine. The lipid content of liver was also determined. On day 4, the lipid content of group 1 was about 45 mg, that of group 2 was about 70 mg, and that of group 3 was about 115 mg (female) and 145 mg (male) per gram of wet weight. Groups 2 and 3 showed significantly higher activity of hepatic malic enzyme than group 1. The activity of intestinal malic enzyme was highest in group 1 and not significantly different between groups 2 and 3. The malic enzyme activity in adipose tissue of females of group 3 was higher than that in either sex of the other groups.
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PMID:Effects of a high fructose diet on lipogenic enzyme activities in some organs of rats fed ad libitum. 118 82


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