palmitic acid/hypoxia

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[Effects of palmitic acid on activity of uncoupling proteins and proton leak in in vitro cerebral mitochondria from the rats exposed to simulated high altitude hypoxia].

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To reveal the roles of uncoupling proteins (UCPs) in disorder of mitochondrial oxidative phosphorylation induced by free fatty acid during hypoxic exposure, the effects of palmitic acid on activity of UCPs, proton leak and mitochondrial membrane potential in hypoxia-exposed rat brain mitochondria

Glucose starvation and hypoxia, but not the saturated fatty acid palmitic acid or cholesterol, activate the unfolded protein response in 3T3-F442A and 3T3-L1 adipocytes.

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Obesity is associated with endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) in adipose tissue. In this study we identify physiological triggers of ER stress and of the UPR in adipocytes in vitro. We show that two markers of adipose tissue remodelling in

Roles and regulation of ketogenesis in cultured astroglia and neurons under hypoxia and hypoglycemia.

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Exogenous ketone bodies (KBs), acetoacetate (AA), and β-hydroxybutyrate (BHB) act as alternative energy substrates in neural cells under starvation. The present study examined the endogenous ketogenic capacity of astroglia under hypoxia with/without glucose and the possible roles of KBs in neuronal

Physiological aspects of the mitochondrial cyclosporin A-insensitive palmitate/Ca2+-induced pore: tissue specificity, age profile and dependence on the animal's adaptation to hypoxia.

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Earlier we found that being added to rat liver mitochondria, palmitic acid (Pal) plus Ca(2+) opened a cyclosporin A-insensitive pore, which remained open for a short time. Apparently, this pore is involved in the Pal-induced apoptosis and may also take part in the mitochondrial Ca(2+) recycling as a

Protective effect of hypoxia on oxygen toxicity: possible mechanisms.

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Previous studies demonstrated a protective effect of hypoxia on subsequent death breathing oxygen. Four groups of rats were exposed to air for 120 hours plus 99% O2 for 52 hours (A + O2); 120 hours of hypoxia plus 52 hours 99% O2 (H + O2); 172 hours of only air (A); and 120 hours of only hypoxia

Acute hypoxic preconditioning prevents palmitic acid-induced cardiomyocyte apoptosis via switching metabolic GLUT4-glucose pathway back to CD36-fatty acid dependent.

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Metabolic syndrome is a risk factor for the development of cardiovascular diseases. Myocardial cell damage leads to an imbalance of energy metabolism, and many studies have indicated that short-term hypoxia during myocardial cell injury has a protective effect. In our previous animal studies, we

Palmitic acid interferes with energy metabolism balance by adversely switching the SIRT1-CD36-fatty acid pathway to the PKC zeta-GLUT4-glucose pathway in cardiomyoblasts.

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Metabolic regulation is inextricably linked with cardiac function. Fatty acid metabolism is a significant mechanism for creating energy for the heart. However, cardiomyocytes are able to switch the fatty acids or glucose, depending on different situations, such as ischemia or anoxia. Lipotoxicity in

Progressive hypoxia inhibits the de novo synthesis of galactosylceramide in cultured oligodendrocytes.

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Neonatal rat oligodendrocyte (OLG) cultures exposed to 6 h of gradual, progressive hypoxia in a GasPak (BBL, Becton Dickinson) apparatus were not injured or metabolically impaired, but instead showed a specific inhibition of de novo synthesis (measured by [3H]palmitic acid labeling) of the major

Experimental conditions affecting in vitro intestinal incorporation of palmitic acid: a methodological approach.

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In the rat, a large number of in vitro studies on intestinal fatty acid uptake have been carried out. However, the results obtained under different experimental conditions are often contradictory. The present work is a critical approach to the experimental aspects which may modify in vitro

Proton leak induced by reactive oxygen species produced during in vitro anoxia/reoxygenation in rat skeletal muscle mitochondria.

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Superoxide anion generation and the impairment of oxidative phosphorylation yield were studied in rat skeletal muscle mitochondria submitted to anoxia/reoxygenation in vitro. Production of superoxide anion was detected after several cycles of anoxia/reoxygenation. Concomitantly, a decrease of state

Effect of hypoxia-reoxygenation on peroxisomal functions in cultured human skin fibroblasts from control and Zellweger syndrome patients.

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To delineate the role of peroxisomes in the pathophysiology of hypoxia-reoxygenation we examined the functions of peroxisomes and mitochondria in cultured skin fibroblasts from controls and from patients with cells lacking peroxisomes (Zellweger cells). The loss of peroxisomal functions (lignoceric

Hydrodynamic and energetic aspects of exogenous free fatty acid perfusion in the isolated rat heart during high flow anoxia and reoxygenation: a 31P magnetic resonance study.

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OBJECTIVE The aim was to show differences between the effects of various dietary long chain fatty acids (palmitic, oleic, linoleic, alpha and gamma linolenic acids) perfused in isolated rat hearts subjected to a sequence of high flow anoxia and subsequent reoxygenation. METHODS Isolated working rat

Mitochondrial apoptosis and curtailment of hypoxia-inducible factor-1α/fatty acid synthase: A dual edge perspective of gamma linolenic acid in ER+ mammary gland cancer.

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Gamma linolenic acid is a polyunsaturated fatty acid having selective anti-tumour properties with negligible systemic toxicity. In the present study, the anti-cancer potential of gamma linolenic acid and its effects on mitochondrial as well as hypoxia-associated marker was evaluated. The effect of

Hypoxia reduces the efficiency of elisidepsin by inhibiting hydroxylation and altering the structure of lipid rafts.

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The mechanism of action of elisidepsin (PM02734, Irvalec®) is assumed to involve membrane permeabilization via attacking lipid rafts and hydroxylated lipids. Here we investigate the role of hypoxia in the mechanism of action of elisidepsin. Culturing under hypoxic conditions increased the

Anti-hypoxia activity and related components of Rhodobryum giganteum par.

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Different extracts of Rhodobryum giganteum Par. were screened with mice model of acute myocardial hypoxia induced by isoproterenol and pituitrin, eight compounds, i.e. p-hydroxycinnamic acid, caffeic acid-4-O-β-d-glucopyranoside, salicin, 7,8-dihydroxy coumarin, menthol, allantoin, palmitic acid,

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