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)

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

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

The effects of one vs. two episodes of starvation-refeeding were studied in young male rats as a function of elapsed time between the two episodes of starvation-refeeding. Starved-refed rats ate more and gained weight faster than ad libitum-fed rats. The difference in weight gains could be attributed to the greater amount of body fat in the starved-refed rats. The responses of four NADP-linked liver dehydrogenases:isocitrate dehydrogenase (ICD)/LS-isocitrate:NADP oxidoreductase (decarboxylating) (EC 1.1.1.42), glucose-6-phosphate dehydrogenase (G6PD)/D-glucose-6-phosphate:NADP oxidoreductase (EC 1.1.1.49); 6-phosphogluconate dehydrogenase (6PGD/6-phospho-D-gluconate:NADP oxidoreductase (decarboxylating) (EC 1.1.1.44); and malic enzyme (ME)/L-malate:NADP oxidoreductase (decarboxylating) (EC 1.1.1.40) were studied. Starvation-refeeding caused an overshoot of G6PD, 6PGD, and ME, but not of ICD. A second episode of starvation caused an even greater enzyme overshoot; this difference persisted for 3 weeks with G6PD and for 2 weeks with 6PGD and ME. No significant differences in blood cholesterol were detected.
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PMID:Long-term effects of starvation-refeeding in the rat. 122 70

For determination of the physiological role and mechanism of vacuolar proteolysis in the yeast Saccharomyces cerevisiae, mutant cells lacking proteinase A, B, and carboxypeptidase Y were transferred from a nutrient medium to a synthetic medium devoid of various nutrients and morphological changes of their vacuoles were investigated. After incubation for 1 h in nutrient-deficient media, a few spherical bodies appeared in the vacuoles and moved actively by Brownian movement. These bodies gradually increased in number and after 3 h they filled the vacuoles almost completely. During their accumulation, the volume of the vacuolar compartment also increased. Electron microscopic examination showed that these bodies were surrounded by a unit membrane which appeared thinner than any other intracellular membrane. The contents of the bodies were morphologically indistinguishable from the cytosol; these bodies contained cytoplasmic ribosomes, RER, mitochondria, lipid granules and glycogen granules, and the density of the cytoplasmic ribosomes in the bodies was almost the same as that of ribosomes in the cytosol. The diameter of the bodies ranged from 400 to 900 nm. Vacuoles that had accumulated these bodies were prepared by a modification of the method of Ohsumi and Anraku (Ohsumi, Y., and Y. Anraku. 1981. J. Biol. Chem. 256:2079-2082). The isolated vacuoles contained ribosomes and showed latent activity of the cytosolic enzyme glucose-6-phosphate dehydrogenase. These results suggest that these bodies sequestered the cytosol in the vacuoles. We named these spherical bodies "autophagic bodies." Accumulation of autophagic bodies in the vacuoles was induced not only by nitrogen starvation, but also by depletion of nutrients such as carbon and single amino acids that caused cessation of the cell cycle. Genetic analysis revealed that the accumulation of autophagic bodies in the vacuoles was the result of lack of the PRB1 product proteinase B, and disruption of the PRB1 gene confirmed this result. In the presence of PMSF, wild-type cells accumulated autophagic bodies in the vacuoles under nutrient-deficient conditions in the same manner as did multiple protease-deficient mutants or cells with a disrupted PRB1 gene. As the autophagic bodies disappeared rapidly after removal of PMSF from cultures of normal cells, they must be an intermediate in the normal autophagic process. This is the first report that nutrient-deficient conditions induce extensive autophagic degradation of cytosolic components in the vacuoles of yeast cells.
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PMID:Autophagy in yeast demonstrated with proteinase-deficient mutants and conditions for its induction. 140 May 75

The maximum activities of some key enzymes of metabolism were studied in lungs of fed and 48-h-starved rats. The maximum activity of hexokinase in the lung is similar to that of other tissues of the body, but lower than that of phosphorylase and 6-phosphofructokinase. High activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase were found in lung tissue, suggesting the importance of the pentose phosphate pathway in the lung. The activities of hexokinase and 6-phosphofructokinase were decreased whereas that of phosphorylase increased in response to starvation. Of the enzymes of the tricarboxylic acid cycle whose activities were measured, that of oxoglutarate dehydrogenase was the lowest, yet its activity (approximately 4.2 nmol/min per mg protein at 37 degrees C) was considerably greater than the flux through the cycle (0.46 nmol/min per mg protein at 37 degrees C; calculated from oxygen consumption by incubated lung slices). The activities of both oxoglutarate dehydrogenase and citrate synthase were decreased by starvation. The activities of 3-oxoacid CoA-transferase and acetoacetyl-CoA thiolase were low in lung tissue compared to those of other tissues (eg kidney, brain) and that of 3-hydroxybutyrate dehydrogenase was very low. The activity of carnitine palmitoyl transferase is higher in the lung, suggesting that fatty acids (and possibly acetoacetate) could provide acetyl-CoA as substrate for the tricarboxylic acid cycle. Very low rates of utilization of 3-hydroxybutyrate were observed during incubation of lung slices, but that of oleate was 1.2 nmol/h per mg of protein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolism of glucose, glutamine, long-chain fatty acids and ketone bodies by lungs of the rat. 176


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