The occurrence of C6–C10-dicarboxylic acids in urine from patients and rats treated with dipropylacetate
References (20)
- et al.
Lancet
(1979) - et al.
FEBS Lett.
(1975) - et al.
Clin. Chim. Acta
(1980) - et al.
Clin. Chim. Acta
(1972) J. Chromatogr.
(1979)Clin. Chim. Acta
(1972)Biochim. Biophys. Acta
(1973)- et al.
Clin. Chim. Acta
(1979) - et al.
Clin. Chim. Acta
(1976) - et al.
Ann. Neurol.
(1979)
Cited by (45)
Non-alcoholic fatty liver disease (NAFLD), insulin resistance and lipid profile in antiepileptic drug treatment
2009, Epilepsy ResearchCitation Excerpt :Animal studies could demonstrate an increase in mitochondrial protein (Hayasaka et al., 1986; Murakami et al., 1990; Sugimoto et al., 1987) and peroxisome proliferation (Draye and Vamecq, 1987; Ponchaut et al., 1991), but an impairment of mitochondrial beta-oxidation of fatty acids (Becker and Harris, 1983; Bjorge and Baillie, 1985). This hypothesis of impaired beta-oxidation is supported by the finding of a reduced availability of Coenzyme A (Melegh et al., 1987), ketone bodies and urinary excretion of dicarboxylic acid (Mortensen et al., 1980). In a state of insulin resistance the intraheptic influx of free fatty acids from adipose tissue is significantly increased, enhancing the risk of intraheptic triglyceride storage (Unger and Orci, 2001).
Weight gain associated with valproate in childhood
2000, Pediatric NeurologySynthesis, purification, and characterization of Dicarboxylylmono- coenzyme A esters
1997, Methods in EnzymologyInhibition of mitochondrial beta-oxidation as a mechanism of hepatotoxicity
1995, Pharmacology and TherapeuticsValproate and mitochondria
1993, Biochemical Pharmacology