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)

In this work the microsomal lauric acid omega-hydroxylation, fatty acid peroxisomal beta-oxidation, and the levels of cytochrome P-450 IVA1 were studied in liver tissue from starved rats. Starvation increased the peroxisomal beta-oxidation and the microsomal hydroxylation of fatty acids. The correlation between these activities would support the proposal that both processes are linked, contributing in part to catabolism of fatty acids in liver of starved rats.
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PMID:Modulation of rat liver peroxisomal and microsomal fatty acid oxidation by starvation. 139 71

Microsomes from the liver of sea bass (Dicentrarchus labrax) were shown to hydroxylate lauric acid at subterminal positions. The cytochrome P-450 system converted lauric acid to several mono-hydroxylated metabolites including omega-1 hydroxylaurate, which was the major metabolite (44% of total products). In addition, omega-2, omega-3, omega-4 and a small amount (2.3%) of omega hydroxylaurates were found. Reaction products were identified using thin-layer chromatography (TLC) and gas chromatography/mass spectrometry (GC/MS). Oxidation reactions were dependent upon O2 and NADPH, and did not occur with boiled microsomes or in the presence of a mixture of CO/O2. Hydroxylation proceeded linearly up to 20 min at 28 degrees C for protein concentrations below 380 micrograms. Treatment of fish with benzo(a)pyrene (BP) (20 mg/kg) drastically increased xenobiotic metabolism (ECOD, EROD and BPMO activities), but no difference in laurate hydroxylase activity was observed between untreated and treated fish. Starvation strongly enhanced laurate hydroxylase activity, and resumption of feeding reduced by half this increase of activity. In all of the experiments we did not observe any modification of the regioselectivity of lauric acid hydroxylation by this microsomal in-chain hydroxylating system. We suggest that cytochrome P-450 enzymes involved in lauric acid and xenobiotics metabolism are regulated independently.
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PMID:Subterminal hydroxylation of lauric acid by microsomes from a marine fish. 152 63

The effects of starvation on rat renal cytochrome P-450s were studied. The content of spectrally measured cytochrome P-450 in the renal microsomes of male rats increased 2-fold with 72 h starvation, but cytochrome b5 and NADPH-cytochrome P-450 reductase were not induced. 7-Ethoxycoumarin O-dealkylation and aniline hydroxylation activities of the renal microsomes of control male rats were very low but were induced 2.5-3-fold by 72 h starvation. Aminopyrine N-demethylation and lauric acid hydroxylation activities were induced 1.5-2-fold by 72 h starvation. The changes in catalytic activities suggested that the contents of individual cytochrome P-450s in the renal microsomes were altered by starvation. The contents of some cytochrome P-450s were measured by Western blotting. P450 DM (P450IIE1), a typical form of cytochrome P-450 induced by starvation in rat liver, was barely detected in rat kidney and was induced 2-fold by 72 h starvation. P450 K-5, a typical renal cytochrome P-450 and lauric acid hydroxylase, accounted for 81% of the spectrally measured cytochrome P-450 in the renal microsomes of control male rats and was induced 2-fold by 72 h starvation. P450 K-5 was not induced in rat kidney by treatment with chemicals such as acetone or clofibrate. The renal microsomes of male rats contained 6-times as much P450 K-5 as those of female rats. These results suggest that P450 K-5 is regulated by an endocrine factor.
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PMID:Induction and regulation of cytochrome P450 K-5 (lauric acid hydroxylase) in rat renal microsomes by starvation. 222 22

The effects of starvation on the composition of 12 different cytochrome P450s in rat hepatic microsomes were studied with a specific antibody. Changes in the metabolic activity of the microsomes were studied at the same time. P450 DM (P450j) was induced 2.5-fold by a 48-h starvation and its increase reflected the increase of metabolic activity of hepatic microsomes toward aniline, 7-ethoxycoumarin, and N-nitrosodimethylamine. P450 K-5, the major renal cytochrome P450 in untreated male rat, was also induced 2.5-fold by a 48-h starvation. P450 UT-2 (P450h) and P450 UT-5 (P450g), typical male-specific forms, decreased with starvation. P450 UT-2 had high testosterone 2 alpha- and 16 alpha-hydroxylation activities. These activities of hepatic microsomes were reduced with the decrease in P450 UT-2. P450 PB-1, testosterone 6 beta-hydroxylase, was increased time-dependently by starvation. P450 UT-4 (RLM2), a minor male-specific form, was not changed by starvation. P450 PB-2 (P450k), present in both sexes, was changed little by starvation. P450 PB-4 (P450b) and P450 PB-5 (P450e) are strongly induced in rat liver by phenobarbital in coordinate fashion. Starvation increased P450 PB-4 12-fold but reduced P450 PB-5 to 22% of the control level. P450 MC-1 (P450d) was decreased by starvation. P450 MC-5 (P450c) was barely detected in control rats and was not changed by starvation. P450 IF-3 (P450a), rich in immature rats, was increased by starvation, accompanied by an increase in testosterone 7 alpha-hydroxylation activity in the hepatic microsomes. We further investigated whether new cytochrome P450s appeared upon starvation by comparison of chromatographic profiles of cytochrome P450 from starved rats with those of cytochrome P450 from control rats using HPLC. Three new cytochrome P450s were detected in the starved rats. These cytochrome P450s were purified to homogeneity. One of them was P450 DM, judging from spectral properties, catalytic activity, and the NH2-terminal sequence. The two other forms were designated P450 3b and 4b. The minimum molecular weights of P450 3b and 4b were 53,000 and 52,000, respectively, and their CO-reduced absorption maxima were at 449 and 452 nm, respectively. P450 3b metabolized aminopyrine, N-nitrosodimethylamine, 7-ethoxycoumarin, and lauric acid, but with low activity. P450 4b was efficient in lauric acid omega- and (omega-1)-hydroxylation only. The spectral properties, catalytic activity, peptide map, and NH2-terminal sequence of P450 4b agreed with those of P450 K-5. P450 3b was a new cytochrome P450, judged by these criteria.
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PMID:Changes in the amount of cytochrome P450s in rat hepatic microsomes with starvation. 232 56

Like Mongolian gerbils (Meriones unguiculatus), Meriones libycus develop an intestinal lipodystrophy due to myo-inositol deficiency. Fat accumulation was observed in the intestine of both species when a myo-inositol-deficient diet containing coconut oil was fed to female gerbils. It began in the duodenum and gradually extended to the entire small intestine. Starvation partially removed the accumulated fats. The efficiency of fat absorption was not affected. Most of the accumulated fats were lauric acid-rich triglyceride with the fatty acid composition reflecting the pattern of the intestinal lymph triglyceride during normal transport of absorbed coconut oil. The ratio of oleic acid to linoleic acid in various intestinal lipids was increased. A marked decrease in all plasma lipid and lipoprotein concentrations, including chylomicron, was also observed. It is assumed that the intestinal fat accumulation resulted from a defect in lymphatic transport of dietary fats.
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PMID:Myo-inositol deficiency in gerbils: comparative study of the intestinal lipodystrophy in Meriones unguiculatus and Meriones libycus. 615 58

Microsomal lauric acid 12-hydroxy lauric acid (omega)-hydroxylation and fatty acid peroxisomal beta-oxidation were studied in kidney tissue from starved rats. Starvation increased the microsomal omega-hydroxylation and peroxisomal beta-oxidation of fatty acids with a high correlation between both processes. Earlier, we reported similar results in liver. Our results support the hypothesis that the role of microsomal fatty acids omega-hydroxylation is the generation of substrate for peroxisomal beta-oxidation, with the final purpose of contributing to a catabolic or gluconeogenic pathway from fatty acids.
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PMID:Starvation effect on rat kidney peroxisomal and microsomal fatty acid oxidation. A comparative study between liver and kidney. 848 69

The results of the present investigation relate the effects of the nutritional state and administration of clofibric acid (CLA), a hypolipidaemic drug and peroxisomal proliferator, on phosphatidylethanolamine (PE) synthesis in rat liver and fatty acid metabolism. Fasting and CLA treatment of animals causes an increase in the amount of PE in endoplasmic reticulum (ER) membranes and mitochondria, as well as in the PE/phosphatidylcholine (PC) ratio. Moreover, the activity of the ethanolamine-specific phospholipid base exchange (PLBE) enzyme in liver ER membranes of fasted animals was enhanced by 75% in comparison to that of animals fed ad libitum. The effect of CLA treatment was additive to that of starvation; PE synthesis tested in vitro via the Ca2+-sensitive PLBE reaction increased 3-fold in comparison to rats fed ad libitum. This is confirmed by an increased Vmax for the reaction, but the affinity of the enzyme for ethanolamine was not significantly changed. These effects were accompanied by an enhanced expression of cytochrome P450 CYP4A1 isoform and elevated activity of the enzyme upon CLA administration. The stimulatory effect of CLA administration on the efficiency of the ethanolamine-specific PLBE reaction can be explained by elimination of lauric acid, a known inhibitor of de novo PE synthesis, during the course of omega-hydroxylation catalysed by CYP4A1, and by increased expression of the PLBE enzyme. The products of omega-hydroxylation of lauric acid, which are then converted by dehydrogenase to 1,12-dodecanedioic acid, did not significantly affect the in vitro synthesis of PE.
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PMID:Positive feedback between ethanolamine-specific phospholipid base exchange and cytochrome P450 activities in rat liver microsomes. The effect of clofibric acid. 973 60

Nutrient-deprived Listeria monocytogenes have increased resistance to processing control measures. Heat-stressed L. monocytogenes cells produce higher counts under anaerobic conditions and SigB reportedly contributes to the survival of environmentally stressed Gram-positive bacteria. In this study, a wild type (wt) strain, L. monocytogenes 10403S, and a DeltasigB mutant, FSLA1-254, were stressed by starvation in phosphate buffered saline coupled with exposure to chemicals with/without oxygen. In the absence of chemicals, the mutant survived starvation almost as well as the wt, suggesting that the starvation survival response (SSR) in L. monocytogenes was SigB-independent. Conversely, in the presence of chemical stresses the SSR results differed depending on the chemical used. In the presence of sodium chloride (SC), both strains were able to express an SSR under aerobic conditions but not under anaerobic conditions. However, in the presence of sodium propionate (SP), the mutant yielded counts that were 2 log CFU/mL lower than the controls and their aerobic counterparts. In the presence of sodium lactate (SL), the mutant yielded counts that were approximately 3 log CFU/mL lower than the wt under anaerobic conditions. Thus, for the chemical stress produced by SC, the SSR appeared to be SigB-independent. The SSR of L. monocytogenes appeared to be SigB-dependent following exposure to SP or SL under anaerobic conditions. Following exposure to sodium diacetate or lauric acid, both strains were unable to express an SSR. No detectable CFUs were observed after 14 to 21 d under either aerobic or anaerobic incubation. Therefore, these 2 chemicals could be used in biocidal formulations against L. monocytogenes cells under aerobic or anaerobic conditions.
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PMID:Resistance of nutrient-deprived Listeria monocytogenes 10403S and a DeltasigB mutant to chemical stresses in the presence or absence of oxygen. 1880 17

Normal and cancerous cells are suggested to have differential utilization of fatty acids and ketone bodies, which could be exploited in cancer therapy. The present study examined the effect of 3-hydroxybutyric acid (3-HBA), which is a ketone body generating acetyl-CoA, and lauric acid (LAA, C12:0), which is a medium-chain saturated fatty acid translocated to mitochondria in a carnitine-independent manner to produce acetyl-CoA, on the energy metabolism of mouse CT26 colon cancer cells. In CT26 cells expressing 3-HBA and LAA transporters, 3-HBA and LAA reduced cell proliferation, mitochondrial volume and lactate production, and increased oxidative stress, particularly in low-glucose conditions. Concurrent treatment with 3-HBA and LAA under glucose starvation had a synergistic effect on cell growth inhibition. In addition, LAA and LAA + 3-HBA promoted an imbalance in the expression of enzymes in the electron transport chain. These findings suggested that treatment with 3-HBA and/or LAA during glucose starvation may reprogram energy metabolism and decrease the proliferation of cancer cells.
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PMID:Remodeling of energy metabolism by a ketone body and medium-chain fatty acid suppressed the proliferation of CT26 mouse colon cancer cells. 2869 20