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)

Compared with traditional techniques of tissue homogenization, digitonin fractionation of isolated hepatocytes provides a much more rapid and, in some instances, more accurate determination of enzyme compartmentation. Results with ATP citrate lyase (EC 4.1.3.8) illustrate the information that uniquely can be obtained. Although the enzyme was previously thought to be entirely cytosolic, digitonin fractionation has shown that a portion of total cellular ATP citrate lyase is bound to mitochondria or some other structure, and the amount bound varies with the animal's nutritional state. In hepatocytes from rats that were starved for 2 days, fed NIH stock diet ab libitum, or starved for 2 days and then refed a fat-free diet for 2 days, the noncytosolic activity was, respectively, 52, 21, or 24% of total cellular lyase. However, because starvation/refeeding greatly induces lipogenic enzymes, the amount of bound lyase activity in this dietary state was 10-12 times greater than that in rats that were starved or fed ad libitum. The association of citrate lyase with a subcellular organelle is also influenced by CoA. Addition of 20 microM CoA to the digitonin fractionation medium caused all of the lyase to be released from cells like a cytosolic enzyme. Conversely, when cellular free CoA was decreased by incubating hepatocytes with the hypolipidemic agent 5-(tetradecyloxy)-2-furoic acid, the amount of bound lyase was increased. These results suggest the possibility that the noncytosolic ATP citrate lyase may have a special role in lipogenesis.
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PMID:Compartmentation of enzymes: ATP citrate lyase in hepatocytes from fed or fasted rats. 398 19

The activity of some NAD- and NADP-dependent dehydrogenases involved in generation of the reducing equivalents for lipogenesis and the activity and some kinetic parameters of ATP-citrate (pro-3S)-lyase from rat liver, i. e. the enzyme involved in the formation of CoASAc, the primary substrate of fatty acid biosynthesis, were studied. The changes in the activity of NADP-dependent dehydrogenase and ATP-citrate(pro-3S)-lyase, as well as the affinity of the latter for sitrate and CoA and the rate of lipogenesis in starved rats and in rats kept on a carbohydrate-rich diet after starvation appeared to be parallel. Nicotinamide decreased the activity of all NADP-dependent dehydrogenases under study, which was especially well-pronounced after nicotinamide addition against increased lipogenesis. The affinity of ATP-citrate(pro-3S)-lyase for citrate and CoA decreased simultaneously with the decrease in the concentration of the latter. These changes can possibly induce the decrease of lipogenesis rate in rat liver after addition of nicotinamide.
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PMID:[Possible mechanisms of the inhibiting effect of nicotinamide on lipogenesis in rat liver]. 645 46

The purpose of the study was to determine the response of liver and brown (BAT) and white (WAT) adipose tissue lipogenesis and total body weight in rats subjected to multiple cycles of 3 days of fasting and 3 days of refeeding. Rats fasted for 3 days showed significant reduction in body weight. These changes were reversed on 3 days' refeeding. Body weight was much higher in rats fed ad libitum than in animals experiencing more than one cycle of 3 days of fasting followed by 3 days of refeeding. Despite the significant body weight reduction, an unusual increase of lipogenesis in WAT was found after multiple cycles of starvation-refeeding of rats on standard laboratory diet. The rate of lipogenesis in the liver and BAT was also elevated but to a much smaller extent. A parallel increase in enzymatic activities related to fatty acid synthesis, ie, fatty acid synthase, acetyl-coenzyme A carboxylase, adenosine triphosphate (ATP)-citrate lyase, NADP-linked malic enzyme, and hexose monophosphate shunt dehydrogenases, suggests that the increased rate of lipogenesis in WAT is a consequence of increased lipogenic enzyme activities. These data suggest that upregulation of WAT lipogenesis occurs after the multiple cycles of the starvation-refeeding protocol. An unusual increase of lipogenesis in rat WAT may have a survival advantage, because starved-refed rats must develop the ability to ingest large amounts of food during a refeeding period to store it in a convenient form than can be used as an oxidizable substrate during a period of starvation. Moreover, these results suggest that it is possible to develop appropriate starvation-refeeding conditions that may inhibit body weight gain.
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PMID:Unususal increase of lipogenesis in rat white adipose tissue after multiple cycles of starvation-refeeding. 900 62

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