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Fatty add metabolism

PPARa GR HNF4a 4A 2B6, 2C9, 3A4, 3A5 2A6, 2B6, 2C9, 2D6, 3 A, 7A1 Fatty add metabolism regulation I m munore sponse regulation Carbohydrate, lipid, protein and... [Pg.320]

The material presented in the preceding sections concerns mainly carbohydrate metabolism during exercise. Before considering fatty add metabolism in exercise, a special carbohydrate should be covered — fructose. [Pg.211]

Catecholamines and Serotonin Appendix Inborn Errors of Amino Acid, Organic Acid, and Fatty Acid Metabolism Inborn Errors of Amino Acid, Organic Acid, and Fatty Add Metabolism Appendix... [Pg.2422]

Chenoweth believes that an explanation of the above results may lie in the reactions occurring before the entrance of fatty acid metabolites into the citric acid cycle. Activated acetate, i.e. acetyl coenzyme A (AcCoA) is the end-product of fatty add metabolism prior to its condensation with oxalacetate to form citrate. Possibly fluoro-fatty acids behave like non-fluorinated fatty acids. The end-product before the oxalacetate condensation could be the same for all three fluorinated inhibitors, viz. fluoroacetyl coenzyme A (FAcCoA). Fluorocitrate could then be formed by the condensation of oxalacetate with FAcCoA, thereby blocking the citric acid cycle. The specificity of antagonisms must therefore occur before entrance of the metabolites into the citric acid cycle. [Pg.166]

Much investigation with diloroacetamides has focused on fatty add metabolism, especially fatty acid elongation to elucidate the mode of adion. [Pg.326]

The Effect of -Oxidabie and Non-P-OxtdabkThia Fatty Adds on Fatty Add Metabolism... [Pg.313]

We and others have recently become interested in the roles aberrant fatty add metabolism may play in the pathogenesis of more common dyslipidemic syndromes such as diabetes, obesity and development of cardiovascular disease. Recent studies reported by Park and coworkers, attempted to identify different genetic backgrounds in mice that... [Pg.400]

Other genes involved in mitochondrial lipid metabolism, such as acyl-CoA synthetase" or medium-chain acyl-CoA dehydrogenase (MCAD), are also targets of PPAR, indicating that different steps of fatty add metabolism, like activation, oxidation, and utilization of fatty acids are regulated by the levels of the substrate, the fatty acids. Therefore, we speculated that the main control step in fatty add P-oxidation, the outer membrane component of carnitine palmitoyltransferase enzyme system, CPT I, could also be a PPAR target. [Pg.80]

Girard, J., Ferre, R, Pegoiier, J. Duee, P. (1992) Physiol. Rev. 72, 507-562 Adaptations of glucose and fatty add metabolism during perinatal period and suclding-weaning transition. [Pg.231]

Asins, G., Rosa, J.L., Serra, D., GU-Gomez, G., Ayte, J., Bartrons, R., Tauler, A. Hegardt, F.G. (1994) Biochem. J. 299, 65-69. Gene expression of enzymes regulating ketogenesis and fatty add metabolism in regenerating rat liver. [Pg.238]

Wanders, R.J.A., Denis, S., Wouteis, R, Wirtz, K.W. Seedorf, U (1997) Biochem. Biophys. Res. Commun. 236, 565-569. Sterol carrier protein X (SCPx) is a peroxisomal branched-chain ()-ketothiolase spedficaUy reacting with 3-oxo-pristanoyl-CoA a new, unique role for SCPx in branched-chain fatty add metabolism in peroxisomes. [Pg.272]

Chloroplasts play a central role in fatty add metabolism in the leaf cell not only do they synthesize fatty acids-and may In fact be the sole site of this synthesis-but they are also able to desaturate fatty acids. Desaturation of 18 0 to 18 1 occurs while the acyl group is esterified to AGP in the stroma the desaturase is a soluble protein, and requires both a source of electrons--reduced ferredoxin is sufficient-and oxygen (Jacobson et al, 1974 Mckeon and Stumpf, 1982). All other fatty acid desaturation in plant cells, in both the plastid and elsewhere, appears to occur while the fatty acids are esterified to glycerolipids (Roughan and Slack, 1982). This is in stark contrast to animal systems In which fatty acids esterified to CoA are the predominant substrates for desaturation. [Pg.181]

Kabir and Kimura fmther investigated the tissue distribution of C-octacosanol in liver and muscle of rats after a series of administrations. They found the highest amoimt of radioactivity in the liver (9.5% of administered dose), followed by the digestive tract (8.2% of administered dose) and the muscle (3.5% of administered dose). Interestingly enough, the radioactivity in the liver disappeared rapidly, while the muscle seemed to be able to store a considerable amount in response to the dose administered. More recently, Menendez et al. demonstrated that octacosanoic acid, as well as short-chain saturated and unsaturated fatty acids, are formed after an oral dosing of policosanol in rats and monkeys. These results reinforce the idea that octacosanol metabolism is linked to fatty add metabolism via P-oxidation. ... [Pg.103]

Carnitine supplementation in these states has proven effective. For example, in cardiac diseases, the myocardium uses fatty acids as its primary source of fuel therefore, a deficiency in carnitine may have a smous impact on heart rate and stroke volume and thus cardiac output. In fact, most research on these types of cardiac patients supports the use of carnitine as a supplement and furthermore has found that abnormal fatty add metabolism is normalized. " The focus of this chapter, however, will be the effects and efficacy of carnitine supplementation in healthy populations, spedfically as a potential eigogenic aid to athletic performance. [Pg.204]

Peroxisome proliferator-activated receptors (PPARs) are a group of nuclear hormone receptors which function as transcription factors in the regulation of genes involved in glucose and lipid fatty add metabolism and vessel wall function. Three PPAR subtypes have been identified PPAR a, y and 8. [Pg.89]

Thus, of the overall 20 metabolic pathways involved in Lipid and Fatty Acid Metabolism, there are 13 such pathways which are exclusively restricted to L. major, of which only 7 pathways had the enzymes and reactions unique to L. major. From the Table 1 it is found that the maximum number of the genes and the resultant gene products (enzymes), distinctive to the L. major are specifically engaged in the LPG and GIPL Biosynthesis Pathway followed by the fatty add metabolism... [Pg.337]

P. K. Stumpf, Fatty add biosynthesis In higher plants. In "Fatty add metabolism and Its regulation," S. Numa, ed., Elsevier Science Publ, Amsterdam (1984)... [Pg.594]

Waldock, M.J. and Holland, D.L. (1984) Fatty add metabolism in young oysters, Crassostrea gigas Polyunsaturated fatty adds. Lipids, 19, 332-336. [Pg.2038]


See other pages where Fatty add metabolism is mentioned: [Pg.117]    [Pg.1713]    [Pg.615]    [Pg.314]    [Pg.378]    [Pg.78]    [Pg.246]    [Pg.411]    [Pg.361]    [Pg.96]    [Pg.226]    [Pg.253]    [Pg.314]    [Pg.378]    [Pg.401]    [Pg.422]    [Pg.301]    [Pg.155]    [Pg.173]    [Pg.361]   
See also in sourсe #XX -- [ Pg.181 ]




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