triacylglycerol/hipoksi

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Hepatic triacylglycerol and fatty-acid biosynthesis during hypoxia in vivo.

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Hepatic fatty acid biosynthesis and the activity of phosphatidate phosphatidate phosphohydrolase, the rate-limiting enzyme of triacylglycerol biosynthesis, were studied after hypoxic periods of 1 and 7 days under hypobaric conditions at 40.8 kPa. Phosphatidate phosphohydrolase activity increased

Cerebral phosphoinositide, triacylglycerol and energy metabolism during severe hypoxia and recovery.

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The cerebral concentrations of phosphatidylinositol (PI), phosphatidylinositol 4-phosphate (PIP), phosphatidylinositol 4,5-bisphosphate (PIP2), phosphatidic acid (PA), triacylglycerol (TAG) and free fatty acids (FFA), as well as cerebral metabolites, were measured in rats subjected to 10 min of

Effect of chronic hypoxia on hepatic triacylglycerol concentration and mitochondrial fatty acid oxidizing capacity in liver and heart.

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The effect of moderated hypoxia (50.5 kPa air) and severe hypoxia (40.8 kPa air) in vivo liver and heart triglyceride concentration and mitochondrial respiration rates was studied. Liver triglyceride concentrations increased in severe hypoxia from 7.3 mumol/g wet weight to 23.3 mumol/g wet weight

Expression of AGPAT2, an enzyme involved in the glycerophospholipid/triacylglycerol biosynthesis pathway, is directly regulated by HIF-1 and promotes survival and etoposide resistance of cancer cells under hypoxia.

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Hypoxia inducible factor-1 (HIF-1) supports survival of normal cells under low oxygen concentration and cancer cells in the hypoxic tumor microenvironment. This involves metabolic reprogramming via upregulation of glycolysis, downregulation of oxidative phosphorylation and, less well documented,

Influence of Serum and Hypoxia on Incorporation of [(14)C]-D-Glucose or [(14)C]-L-Glutamine into Lipids and Lactate in Murine Glioblastoma Cells.

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Glucose and glutamine are essential energy metabolites for brain tumor growth and survival under both normoxic and hypoxic conditions. Both metabolites can contribute their carbons to lipid biosynthesis. We used uniformly labeled [(14)C]-U-D-glucose and [(14)C]-U-L-glutamine to examine the profile

Modeling phenotypic metabolic adaptations of Mycobacterium tuberculosis H37Rv under hypoxia.

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The ability to adapt to different conditions is key for Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), to successfully infect human hosts. Adaptations allow the organism to evade the host immune responses during acute infections and persist for an extended period of time

Identification and characterisation of small-molecule inhibitors of Rv3097c-encoded lipase (LipY) of Mycobacterium tuberculosis that selectively inhibit growth of bacilli in hypoxia.

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The mycobacterial Rv3097c-encoded lipase LipY is considered as a true lipase involved in the hydrolysis of triacylglycerol stored in lipid inclusion bodies for the survival of dormant mycobacteria. To date, orlistat is the only known LipY inhibitor. In view of the important emerging role of this

The effect of anoxia on lipid metabolism in isolated adult rat cardiac myocytes.

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In ischemic myocardium abnormal lipid metabolism results in accumulation of compounds that are deleterious to membrane structural integrity and membrane dependent functions. In this study isolated adult rat ventricular myocytes were used to investigate anoxia-induced alterations in cellular lipid

Hormones and triacylglycerol metabolism under normoxic and ischemic conditions.

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Fatty acids, the preferred substrate in normoxic myocardium, are derived from either exogenous or endogenous triacylglycerols. The supply of exogenous fatty acids is dependent of the rate of lipolysis in adipose tissue and of the lipoprotein lipase activity at the coronary vascular endothelium. A

Studies on the plasma cholesterol and triacylglycerols in chronic methemoglobinemia in rats.

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Plasma cholesterol and triacylglycerols were measured in rats with modelled chronic two-stage (mild and moderate) intermittent nitrite methemoglobinemia for 15 and 30 days. It was found that at the moment of methemoglobinemic peak (60 +/- 10 min) the experimental animals had mixed (hemtoxic, anemic

Triacylglycerol utilization is required for regrowth of in vitro hypoxic nonreplicating Mycobacterium bovis bacillus Calmette-Guerin.

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Mycobacteria store triacylglycerols (TGs) under various stress conditions, such as hypoxia, exposure to nitric oxide, and acidic environments. These stress conditions are known to induce nonreplicating persistence in mycobacteria. The importance of TG accumulation and utilization during regrowth is

Effects of maternal iron restriction in the rat on hypoxia-induced gene expression and fetal metabolite levels.

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The mechanism by which maternal Fe deficiency in the rat causes fetal growth retardation has not been clearly established. This study compared the effects on the fetuses from dams fed a control diet with two groups of dams fed Fe-restricted diets. One Fe-restricted group was fed the Fe-restricted

Effects of fasting, hypoxia, methylpalmoxirate and oxfenicine on the tissue-levels of long-chain acyl CoA and acylcarnitine in the rat atria.

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During hypoxia the atria from fasted rats exhibit a faster decline in the pacemaker and contractile activities than those from fed rats. Oxfenicine and methylpalmoxirate, inhibitors of carnitine palmitoyltransferase 1 (CPT 1), ameliorate these disturbances. Since the fasted rat atria have greater

Effect of hypoxia on phospholipid metabolism in porcine pulmonary artery endothelial cells.

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The effect of exposure of porcine pulmonary artery endothelial cells to hypoxic (0% O2) and normoxic (20% O2) conditions for 24 and 48 h on phospholipid metabolism was studied. Sonicates prepared from endothelial cells that were exposed to 24 h of hypoxia showed significant increases in

Possible pathomechanisms of sudden infant death syndrome: key role of chronic hypoxia, infection/inflammation states, cytokine irregularities, and metabolic trauma in genetically predisposed infants.

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Chronic hypoxia, viral infections/bacterial toxins, inflammation states, biochemical disorders, and genetic abnormalities are the most likely trigger of sudden infant death syndrome (SIDS). Autopsy studies have shown increased pulmonary density of macrophages and markedly more eosinophils in the

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