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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mitochondrial and peroxisomal fatty acid oxidation were compared in whole liver homogenates. Oxidation of 0.2 mM palmitoyl-CoA or oleate by mitochondria increased rapidly with increasing molar substrate:albumin ratios and became saturated at ratios below 3, while peroxisomal oxidation increased more slowly and continued to rise to reach maximal activity in the absence of albumin. Under the latter condition mitochondrial oxidation was severely depressed. In homogenates from normal liver peroxisomal oxidation was lower than mitochondrial oxidation at all ratios tested except when albumin was absent. In contrast with mitochondrial oxidation, peroxisomal oxidation did not produce ketones, was cyanide-insensitive, was not dependent on carnitine, and was not inhibited by (+)-octanoylcarnitine, malonyl-CoA and 4-pentenoate. Mitochondrial oxidation was inhibited by CoASH concentrations that were optimal for peroxisomal oxidation. In the presence of albumin, peroxisomal oxidation was stimulated by Triton X-100 but unaffected by freeze-thawing; both treatments suppressed mitochondrial oxidation. Clofibrate treatment increased mitochondrial and peroxisomal oxidation 2- and 6- to 8-fold, respectively. Peroxisomal oxidation remained unchanged in starvation and diabetes. Fatty acid oxidation was severely depressed by cyanide and (+)-octanoylcarnitine in hepatocytes from normal rats. Hepatocytes from clofibrate-treated rats, which displayed a 3- to 4-fold increase in fatty acid oxidation, were less inhibited by (+)-octanoylcarnitine. Hydrogen peroxide production was severalfold higher in hepatocytes from treated animals oxidizing fatty acids than in control hepatocytes. Assuming that all H2O2 produced during fatty acid oxidation was due to peroxisomal oxidation, it was calculated that the contribution of the peroxisomes to fatty acid oxidation was less than 10% both in cells from control and clofibrate-treated animals.
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PMID:Mitochondrial and peroxisomal fatty acid oxidation in liver homogenates and isolated hepatocytes from control and clofibrate-treated rats. 43 7

The effect of clofibrate treatment on hepatic ketogenic capacity was studied in rats. Ketogenesis from octanoate and oleate was increased 2- and 4,5-fold, respectively, in hepatocytes from fed, treated rats. In contrast to controls ketogenic rates did not increase upon starvation. While ketogenesis from oleate was higher in fed, treated animals than in fasted controls, endogenous ketogenesis was lower and increased upon starvation. Ketogenesis from octanoate and oleate was stimulated approx. 2-fold in homogenates from treated animals. Labeled pyruvate and succinate oxidation was unaltered. [1-14C]Oleate oxidation was severely inhibited by cyanide, both in homogenates from controls and treated animals. Clofibrate caused a 3-fold increase in hepatic carnitine levels. Catalase and glutamate dehydrogenase activities were also increased by the drug. Cytochrome c oxidase did not change. Despite their increased ketogenic capacity hepatocytes from treated rats esterified as much oleate as controls. The increased oxidation was matched by an increased oleate uptake. Plasma ketones were increased 2-fold in fasted, treated animals. Plasma free fatty acids were unaffected. It is concluded that the enhanced ketogenic capacity induced by clofibrate is the result of an increase in mitochondrial beta-oxidation, an increase in the activity of carnitine palmitoyltransferase and possibly of the observed increases in hepatic carnitine content and fatty acid uptake.
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PMID:Hepatic fatty acid oxidation and ketogenesis after clofibrate treatment. 65 51

Adult male mice of the NMRI strain were treated with a diet containing 0.5% clofibrate for 4 days to study its effects on peroxisomes, mitochondria, and lipid droplets in hepatocytes. Animals were also starved overnight to study the additional effects of starvation. Starvation of control animals had small effects on peroxisomes while the mitochondria became enlarged and occupied more of the cytoplasm. The number and fractional area of lipid droplets increased fivefold. Clofibrate treatment caused a doubling in number and average size of peroxisomes. No significant effects were observed in the number of mitochondrial profiles or lipid droplets although the size of the latter decreased to a third the value of the fed control. Starvation of clofibrate-treated animals led to a slight increase in the number of peroxisomes although their average size decreased by 30%. Mitochondrial average area increased and their fractional cytoplasmic area increased despite the decrease in numerical density. The number of lipid droplets increased twofold compared to that of clofibrate-treated animals while the size was not affected.
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PMID:Effects of clofibrate treatment and of starvation on peroxisomes, mitochondria, and lipid droplets in mouse hepatocytes: a morphometric study. 262 78

Fatty acid-binding capacity of dealbuminized, delipidated cytosolic proteins from rat tissues was studied with a radiochemical binding assay. Oleate-binding capacity ranges from 1.6 to 4.4 pmol/micrograms cytosolic protein in liver, heart, kidney, adrenal, brain, skeletal muscle and diaphragm. Differences in binding affinity indicate the presence of different fatty acid-binding proteins in these tissues. No change in fatty acid-binding protein content of heart and liver cytosol was observed during postnatal development up to 70 days. Starvation did not affect the fatty acid-binding capacity of heart cytosol, but increased the oleate-binding capacity in liver cytosol. Sex-related differences of binding by heart and liver cytosolic proteins were found with oleate, but not with palmitate. Fatty acid-binding capacity of liver and heart cytosol did not show marked diurnal variation. Clofibrate treatment had different effects on the oleate-binding capacity of cytosolic proteins: an increase in liver and kidney, no change in skeletal muscle and a decrease in heart. The results are discussed in relation to data concerning fatty acid oxidation.
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PMID:Fatty acid-binding capacity of cytosolic proteins of various rat tissues: effect of postnatal development, starvation, sex, clofibrate feeding and light cycle. 373 Apr 5

Whole cells, homogenates and mitochondrial obtained from the livers of albino rats which were starved for 6 days or more showed a 50% decrease in oxidative activity. The decrease could be corrected by the addition of cytochrome c in vitro. The phosphorylative activity of mitochondria remained unaffected. The decrease in oxidative rate was not observed when starving animals were given the anti-hypercholesterolaemic drug clofibrate. The total cellular concentration of cytochrome c was not affected by starvation. However, the concentration of the pigment in hepatic mitochondria isolated from starving animals was less than half that in normal mitochondria. Clofibrate-treated animals did not show a decreased concentration of cytochrome c in hepatic mitochondria. Mitochondria isolated from starving animals, though deficient in cytochrome c, did not show any decrease in succinate dehydrogenase activity or in the rate of substrate-dependent reduction of potassium ferricyanide or attendant phosphorylation. In coupled mitochondria, ferricyanide may not accept electrons from the cytochrome c in the respiratory chain. Starvation decreases the concentration of high-affinity binding sites for cytochrome c on the mitochondrial membrane. The dissociation constant increases in magnitude.
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PMID:Influence of starvation and clofibrate administration on oxidative phosphorylation by rat liver mitochondria. 625 42

Oxidation rates of palmitate (total and antimycin-insensitive), pyruvate, leucine, 4-methyl-2-oxopentanoate and 3-methyl-2-oxobutanoate and activities of two mitochondrial marker enzymes (citrate synthase and cytochrome c oxidase) were assayed in liver and muscle homogenates of fed, clofibrate-treated and 18 hr-starved rats. Significant alterations in the clofibrate-treated and the starved rats were predominantly observed in the liver. Clofibrate feeding increased antimycin-insensitive (peroxisomal) and antimycin-sensitive (mitochondrial) palmitate oxidation and 4-methyl-2-oxopentanoate and pyruvate oxidation in liver. In muscle, only the activities of citrate synthase and cytochrome c oxidase were slightly decreased. Short starvation increased antimycin-sensitive palmitate and 4-methyl-2-oxopentanoate oxidation in liver. The rates of pyruvate and 3-methyl-2-oxobutanoate oxidation were decreased in muscle homogenates. Results suggest that myopathic phenomena observed after chronic clofibrate administration are not related to changes in the capacity of oxidative metabolism of muscle.
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PMID:Effect of clofibrate feeding on palmitate and branched-chain 2-oxo acid oxidation in rat liver and muscle. 631 Dec 21

Severe seasickness could pose a serious problem in diving, and anti-seasickness medication should therefore be prescribed for the seasickness-susceptible diver. Cinnarizine may be used as a medication if it does not increase the risk of central nervous system (CNS) oxygen toxicity when diving with closed-circuit oxygen or O2-enriched gas mixtures. Twenty-six male, white Sprague-Dawley rats were exposed to high O2 pressures (507 and 608 kPa) before and after cinnarizine ingestion (3.3 mg.kg-1), until the appearance of the first electrical discharge (FED) in the electroencephalogram (EEG) which precedes the clinical convulsions. Each rat was tested on five exposure protocols (control and cinnarizine at 507 kPa O2, control, cinnarizine, and 15 h starvation as a control for cinnarizine at 608 kPa O2) at intervals of at least 2 days or until the EEG connector became detached (a mean of 3.1 exposures per rat). Latency to the FED increased after cinnarizine ingestion in 16 of the 17 pairs of measurements at 507 kPa O2 (by more than 61%, P < 0.002) and in 17 of the 19 pairs of measurements at 608 kPa O2 (by 36%, P < 0.002). There was no significant effect of 15 h starvation. Cinnarizine can be further considered for use in seasickness-susceptible divers as it does not increase the risk of CNS O2 toxicity.
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PMID:Effect of the anti-motion-sickness medication cinnarizine on central nervous system oxygen toxicity. 1037 30

The development of genetic sexing strains (GSSs) based on classical genetic approaches has revolutionized the application of the sterile insect technique (SIT) against the Mediterranean fruit fly Ceratitis capitata (Wiedemann) (Diptera: Tephritidae). The global use of Mediterranean fruit fly GSS for SIT applications as part of area-wide integrated pest management (AW-IPM) programmes is testimony to their effectiveness. During recent years, transgenic sexing strains (TSSs) have been developed through genetic engineering techniques offering the possibility to produce male-only progeny by introducing female embryonic lethal genes and to increase the efficacy to identify released sterile males by means of the expression of fluorescent transgene markers. Here, we present a comparative analysis of two Mediterranean fruit fly strains: the classical GSS VIENNA 8D53-/Toliman and the transgenic FSEL#32. The strains were compared for production efficiency and quality control indices under semi mass-rearing conditions, response to sterilizing irradiation doses, male mating performance in walk-in field cages, and production cost of male-only pupae. The results showed that, the FSEL #32 TSS had a similar fecundity but a higher production of male-only pupae than the VIENNA 8D53-/Toliman GSS. For some of the quality control parameters tested, such as pupal weight and survival under starvation conditions, the FSEL #32 TSS was inferior to the VIENNA 8D53-/Toliman GSS. Both the transgenic and the classical genetic sexing strains have shown acceptable and similar mating competitiveness when compared with wild males for mating with wild females. The cost production for both strains is similar but the FSEL#32 TSS may potentially be more cost effective at higher production levels. The results are discussed in the context of incorporating the transgenic strain for SIT application.
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PMID:Comparison of classical and transgenic genetic sexing strains of Mediterranean fruit fly (Diptera: Tephritidae) for application of the sterile insect technique. 3055 May 98