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 interacting effects of diet and glucocorticoid (GC) on the tritium incorporation into lipid and glucose-6-phosphate dehydrogenase activity in starved-refed rats was studied. Male Sprague-Dawley rats were intact, adrenalectomized (ADX), or ADX and given GC and fed either ad libitum or not fed for 48 hours amd refed either a 65% glucose diet, 65% sucrose diet, 65% starch diet, 65% protein diet or a 40% fat diet. No diet differences in rates of 3HOH incorporation into total lipids were observed in ad libitum-fed rats. ADX lowered lipogenesis and this effect was diet dependent. Sucrose-fed, glucose-fed and protein-fed ADX rats had lower rates of lipogenesis than their intact controls. Starvation-refeeding increased lipogenesis in all groups of intact rats except those fed the 40% fat diet. The magnitude of the response was diet dependent. Sucrose-fed rats had greater responses than fat-fed rats. The diet effect was dependent on the presence of the adrenals and GC. Thus, the large increase in liver lipid associated with starvation-refeeding is contingent on the composition of the diet and the presence of the adrenals.
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PMID:Effects of diet composition and adrenalectomy on the lipogenic responses of rats to starvation-refeeding. 706 47

Male inbred Fischer rats were fed a diet containing 5 p.p.m. aflatoxin for 1, 3, 4 1/2 and 6 weeks at which times groups were killed for histological and histochemical study. Aflatoxin produced a scattered individual cell necrosis of parenchymal cells by 1 week. At 3 weeks small basophilic proliferative foci were seen which increased in size and abundance to 6 weeks. These foci showed starvation-resistant glycogen, variable depletion of glucose-6-phosphatase, succinic dehydrogenase, aniline hydrogenase, membrane ATPase and acid phosphatase. At 6 weeks the foci showed the presence of gamma glutamyl transpeptidase and glucose-6-phosphate dehydrogenase. The basophilic foci were not preceded by other focal histological and histochemical change. The basophilic proliferative lesions are observed when an irreversible change has been induced in the liver. The role of such lesions in the histogenesis of hepatocellular carcinoma is discussed.
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PMID:Histochemical studies on the early proliferative lesion induced in the rat liver by aflatoxin. 724 Dec 69

Liver glucose-6-phosphate dehydrogenase (G6PD, EC 1.1.1.49) and malic enzyme (ME, EC 1.1.1.40) activities were measured in rats that were starved for 2 days and then fed a high-glucose, adequate-protein diet for 3 days. During refeeding the rats were injected with thyroxine to block glycogen accumulations preceeding the enzyme "overshoot". The G6PD and ME "overshoot" at the end of refeeding was still evident in spite of a 90% reduction in the glycogen peak. The results showed that the glycogen accumulation prior to the enzyme "overshoot" was not obligatory to the subsequent rise in enzyme activity. The sequential accumulation/breakdown of liver glycogen (day 1 refeeding) followed by the accumulation of liver fat (day 2 of refeeding) are probably the result of the changes in enzymatic pathways available to deal with the inflow of excess glucose. Such dissociation of glycogen accumulation and G6PD and ME "overshoot" during starvation-refeeding makes it highly unlikely that either glucose or glucose-6-phosphate derived from glycogen would be the direct, primary inducer of G6PD or ME in rat liver.
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PMID:Induction of rat liver glucose-6-phosphate dehydrogenase and malic enzyme during blockage of glycogen accumulation. 744 69

The great increase ("overshoot") in glucose-6-phosphate dehydrogenase activity in liver cytoplasm which follows the transfer of rats from starvation to a high sucrose diet has been recognized for a number of years. Also the fact that transferring fed rats to the high sucrose diet results only in a small increase in G6PD activity while transfer of "starved" rats to the high sucrose diet results in a 10 to 20-fold ("overshoot") increase in G6PD activity is equally recognized. This report demonstrates that the "overshoot" following 4 days without food is not due to an increase in food intake compared to the food intake of fed rats since pair-feeding during this refeeding at three different levels does not eliminate the effect of the prior fast.
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PMID:Pair-feeding in the dietary control of glucose-6-phosphate dehydrogenase. 746 69

In the present study we observed that the cerebral glucose-6-phosphate dehydrogenase activity of male garden lizards did not change appreciably during maturation but showed a significant rise between middle-aged and old-aged groups. Whereas cold stress (1 h at 0-4 degrees C) induced a significant increase in G6PDH activity of young animals, it caused a decrease in both middle-aged and old lizards. This decrease was more severe in the old group than in the middle-aged group. Another form of stress, 72 hours of starvation, led to a significant increase in enzyme activity in young and in middle-aged lizards with young animals showing the greater effect. The old counter-parts showed a decrease in enzyme activity after starvation stress.
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PMID:Effect of cold stress and starvation on the cerebral glucose-6-phosphate dehydrogenase activity of male garden lizards of three different age groups. 832 88

The time courses of gene expression, and the nutritional regulation of gene expression of lipogenic enzymes (acetyl-CoA carboxylase, fatty acid synthase, ATP citrate-lyase, malic enzyme, and glucose-6-phosphate dehydrogenase) in epididymal adipose tissue after refeeding food-deprived rats have been investigated and compared with those in liver (previously reported). The mRNA concentrations of lipogenic enzymes reached maximum levels at 24 h after the refeeding in adipose tissue and at 8-16 h in liver, while the enzyme induction reached maximum at 48-72 h in both tissues. Moreover, the mRNAs were more strongly induced in adipose tissue than in liver, whereas the enzyme induction (except malic enzyme) was lower. In adipose tissue of rats fed a carbohydrate diet without protein, the mRNA concentrations of acetyl-CoA carboxylase, ATP-citrate lyase, malic enzyme, and fatty acid synthase reached comparable levels to those of the carbohydrate/protein diet group. The protein feeding increased the enzyme induction in adipose tissue. As regards reduction of gene expression, lipogenic enzyme mRNA concentrations were not so markedly reduced by starvation or polyunsaturated fatty acids in adipose tissue as in liver. The differences in regulation of lipogenic enzyme gene expression and induction between adipose tissue and liver can be ascribed to tissue specificity.
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PMID:Nutritional regulation of lipogenic enzyme gene expression in rat epididymal adipose tissue. 888 6

Herein we report on the kinetic and protein expression of glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase, and malic enzyme (ME) in the liver of the trout (Oncorhynchus mykiss) during a long-term starvation-refeeding cycle. Starvation significantly depressed the activity of these enzymes by almost 60%, without changing the Michaelis constant. The time response to this nutritional stimulus increased with fish weight. The sharp decline in G6PDH and ME activities was due to a specific protein-repression phenomenon, as demonstrated by molecular and immunohistochemical analyses. Also, the dimeric banding pattern of liver G6PDH shifted from the fully reduced and partially oxidized forms, predominant in control, to a fully oxidized form, more sensitive to proteolytic inactivation. Refeeding caused opposite effects in both protein concentration and enzyme activities of about twice the control values in the first stages, later reaching the normal enzyme activity levels. Additionally, the partially oxidized form of G6PDH increased. The kinetics of these enzymes were examined in relation to the various metabolic roles of NADPH. These results clearly indicate that trout liver undergoes protein repression-induction processes under these two contrasting nutritional conditions.
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PMID:Impact of starvation-refeeding on kinetics and protein expression of trout liver NADPH-production systems. 960 11

1. The effects of dietary polychlorinated biphenyls (PCBs) (30-2000 ppm) on activities of gluconeogenic (phosphoenolpyruvate carboxykinase-PEPCK, and fructose 1,6-bisphosphatase-FdPase) and lipogenic enzymes (fatty acid synthase-FAS, ATP citrate lyase-ACL, malic enzyme-ME, glucose 6-phosphate dehydrogenase-G6PDH, and 6-phosphogluconate dehydrogenase-PGDH) were studied in livers of the female Sprague-Dawley and Wistar rat. 2. PCB amounts accumulating in the liver reflected the extent of dietary exposure. The Wistar strain was more sensitive to PCBs than the Sprague-Dawley strain. Of the Clophentype PCBs those containing 60 and 64% chlorine displayed the most pronounced effects. 3. Activities of gluconeogenic enzymes (PEPCK and FdPase) were dose-dependently decreased by PCBs, PEPCK being considerably more sensitive. This decrease was also found under conditions where the activity of PEPCK was induced (administration of adrenalin, glucagon or cAMP, feeding high protein diets, starvation). 4. Activities of lipogenic enzymes were induced by PCBs. The increase was much greater with ME, G6PDH and PGDH (up to 10-fold) than with FAS and ACL (approximately 2-fold). PCB effects were dose-dependent, but transient. 5. In cultured hepatocytes basal activities of lipogenic enzymes were induced by PCBs in the absence of hormones. With saturating levels of insulin or triiodothyronine, enzyme activities were also induced, but addition of PCBs resulted in an additive effect. 6. These results suggest that in the female rat PCBs can mimic the actions of certain hormones by affecting either hormone levels, hormone receptor systems or regulatory systems.
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PMID:Polychlorinated biphenyls affect the activities of gluconeogenic and lipogenic enzymes in rat liver: is there an interference with regulatory hormone actions? 962 50

Expression of glucose-6-phosphate dehydrogenase (G6PD) gene during starvation and refeeding is regulated by a posttranscriptional mechanism occurring in the nucleus. The amount of G6PD mRNA at different stages of processing was measured in RNA isolated from the nuclear matrix fraction of mouse liver. This nuclear fraction contains nascent transcripts and RNA undergoing processing. Using a ribonuclease protection assay with probes that cross an exon-intron boundary in the G6PD transcript, the abundance of mRNAs that contain the intron (unspliced) and without the intron (spliced) was measured. Refeeding resulted in 6- and 8-fold increases in abundance of G6PD unspliced and spliced RNA, respectively, in the nuclear matrix fraction. However, the amount of G6PD unspliced RNA was at most 15% of the amount of spliced RNA. During refeeding, G6PD spliced RNA accumulated at a rate significantly greater than unspliced RNA. Further, the amount of partially spliced RNA exceeded the amount of unspliced RNA indicating that the enhanced accumulation occurs early in processing. Starvation and refeeding did not regulate either the rate of polyadenylation or the length of the poly(A) tail. Thus, the G6PD gene is regulated during refeeding by enhanced efficiency of splicing of its RNA, and this processing protects the mRNA from decay, a novel mechanism for nutritional regulation of gene expression.
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PMID:Regulation of the processing of glucose-6-phosphate dehydrogenase mRNA by nutritional status. 1112 67

Recently, we have found that despite the significant reduction of body weight after multiple starvation-refeeding cycles, white adipose tissue (WAT) exhibits surprisingly high rates of lipogenesis and lipogenic enzyme activities. The purpose of this study was to determine the response of WAT lipogenic enzyme mRNAs of rats subjected to multiple cycles of 3 days fasting and 3 days of refeeding. Despite the body weight reduction, significant increase of lipogenic enzymes (ie, fatty acid synthase [FAS], acetyl-coenzyme A [CoA] carboxylase [ACC], adenosine triphosphate (ATP)-citrate lyase [ACL], NADP-linked malic enzyme [ME], and glucose 6-phosphate dehydrogenase [G6PDH]) mRNAs in WAT was found after multiple cycles of starvation-refeeding of rats on standard laboratory diet. These findings, together with the results published recently, indicate that multiple cycles of starvation-refeeding cause the increased lipogenesis in WAT by upregulation of the lipogenic enzymes gene expression.
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PMID:Increase of lipogenic enzyme mRNA levels in rat white adipose tissue after multiple cycles of starvation-refeeding. 1139 54


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