Beta-oxidation, of fatty acids

Mortensen PB. C6-C10-dicarboxyUc aciduria in starved, fat-fed and diabetic rats receiving decanoic acid or medium-cbain triacylglycerol. An in vivo measure of the rate of beta-oxidation of fatty acids. Biochim BiophysActa, 1981, 664(2), 349-355. 

Wood PA Defects in mitochondrial beta-oxidation of fatty acids. CurrOpin Lipidol 1999 10 107. 

Labbe, G. et al. (1991) Effects of various tetracycline derivatives on in vitro and in vivo beta-oxidation of fatty acids, egress of triglycerides from the liver, accumulation of hepatic triglycerides, and mortality in mice. Biochemical Pharmacology, 41 (4), 638-641. 

Side effects. The common dose-related side effects of valproate include nausea, vomiting and gastrointestinal distress weight gain is frequent (estimated as high as 30%) and may be associated with a drug-induced decrease in the beta oxidation of fatty acids. Sedation is also frequent. Alopecia is an unusual side effect of valproate, possibly caused by an abnormal metabolite. Valproate has a number of metabolically linked side... 

The authors suggested that this patient had a defect in lipid metabolism, based on the muscle biopsy. Muscle mitochondria are a principle site for beta-oxidation of fatty acids. Microvesicular steatosis can progress to liver failure with severe and prolonged impairment of beta-oxidation. This metabolic defect may have exacerbated the direct toxic effects of cocaine. 

Yonssef JA, Song WO, and Badr MZ (1997) Mitochondrial, bnt not peroxisomal, beta-oxidation of fatty acids is conserved in coenzyme A-deflcient rat liver. Molecular and Cellular Biochemistry 175,37-42. 

There are several drugs that inhibit beta oxidation of fatty acids in mitochondria leading to lipid accumulation, such as aspirin, valproic acid, and tetracyclines. 

In eucaryotic cells beta oxidation of fatty acids occurs in the... 

The year 23004 marked the centenary of two important discoveries in the field of metabolism The discovery of beta-oxidation of fatty acids by Franz Knoop (1904), and the discovery of the oxygen dependence for normal pump function of the heart by Hans Winterstein (1904).2 The year 2004 also marked the 50th anniversary of the discovery, by Richard Bing and his colleagues, that the human heart prefers fatty acids for respiration.3... 

Kunau, W.-H., Dommes, V., Schulz, H. 1995. Beta oxidation of fatty acids in mitochondria, peroxisomes, and bacteria a century of continued progress. Prog. Lipid Res. 34 267-341. 

Some of the causes of hepatotoxicity outlined by Lee (2003) include covalent binding of xenobiotics mediated by cytochrome P450s alterations of mitochondrial function affecting beta-oxidation of fatty acids ... 

The structure of cholesterol suggests that its synthesis involves multimolecular interactions yet all of the 27 carbons are derived from one precursor, acetyl CoA. Acetyl CoA can be obtained from several sources, including the beta oxidation of fatty acids, the oxidation of ketogenic amino acids, such as leucine and lysine, and the pyruvate dehydrogenase reaction. Carbons 1, 2, 5, 7, 9, 13, 15, 18, 19, 20, 22, 24, 26, and 27 of cholesterol are derived from the methyl group of acetyl CoA and the remaining 12 carbons of cholesterol from the carboxylate atom of acetyl CoA. 

Rahman, SM., Wang, Y.M., Yotsumoto, H., Cha, J.Y, Inoue, S., and Yanagita, T. (2001) Effects of Conjugated Linoleic Acid on Serum Leptin Concentration, Body Fat Accumulation and Beta-Oxidation of Fatty Acid in OLETF Rats, Nutrition 17,385-390. 

Schulz, H. (1991) Beta-Oxidation of Fatty Acid, Biochim. Bio-phys.Acta 1081,109-120. 

Schulz H. Beta oxidation of fatty acids. Biochim Biophys Acta. 1991 1081(2) 109-20. 

Effects of Conjugated Linoleic Acid on Serum Leptin Concentration, Body-Fat Accumulation, and Beta-Oxidation of Fatty Acid in OLETF Rats, Nutrition 17 385—390 (2001). 

Acetyl-CoA. There is a key metabolite of energy metabolism. It is produced in mitochondria by decarboxylation of pyruvate, beta oxidation of fatty acids, or hydrolysis of acetoacetate. In condensation reaction with oxaloacetate, acetyl-CoA yields citrate, which is the first intermediate in the tricarboxylic acid chain. Acetyl-CoA is also used for the synthesis of acetylcholine and the acetylation of several low molecular weight compounds and proteins. In liver and adipose tissue, acetyl-CoA is used for the synthesis of the fatty acids chain. 

Liver The pathogenesis and clinical characteristics of drug-induced liver injury associated with antiepileptic drugs has been reviewed [41 ]. Reactive metabolites can, in some cases, lead to direct cytotoxicity and liver cell necrosis, whereas in other cases they can cause neoantigen formation, inducing immunoallergic mechanisms. In fact, hypersensitivity features are found in more than 70% of patients with pheny-toin-induced liver injury, whereas this is only observed in 30% of carbamazepine-associated hepatotoxicity and very rarely with valproate-induced liver injury. No specific therapy is of proven value in these cases. However, carnitine, which is an important co-factor in mitochondrial beta-oxidation of fatty acids, is recommended in valproate-associated liver injury, and N-acetylcysteine is an appropriate treatment in patients with liver injury due to pheny-toin and carbamazepine. Liver transplantation may be required for patients with the most severe liver reactions. 

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