1990
DOI: 10.1016/s0006-291x(05)80200-1
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Regulation by induction of branched-chain 2-oxo acid dehydrogenase complex in clofibrate-fed rat liver

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Cited by 15 publications
(25 citation statements)
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“…However, it is clear that clofibrate treatment promotes BCAA catabolism in the whole body of rats by activation of BCKDC, especially in liver and skeletal muscle, as reported previously (Kobayashi et al, 2002;Ono et al, 1990;Paul and Adibi, 1980). Thus, increased BCKDC activity influences the plasma BCAA concentrations (i.e., concentrations of the three BCAAs were significantly decreased by clofibrate treatment).…”
Section: Discussionsupporting
confidence: 69%
See 1 more Smart Citation
“…However, it is clear that clofibrate treatment promotes BCAA catabolism in the whole body of rats by activation of BCKDC, especially in liver and skeletal muscle, as reported previously (Kobayashi et al, 2002;Ono et al, 1990;Paul and Adibi, 1980). Thus, increased BCKDC activity influences the plasma BCAA concentrations (i.e., concentrations of the three BCAAs were significantly decreased by clofibrate treatment).…”
Section: Discussionsupporting
confidence: 69%
“…It has been reported that clofibric acid, an active metabolite of clofibrate, activates BCKDC and therefore increases the rate of leucine oxidative disposal (Kobayashi et al, 2002;Ono et al, 1990;Paul and Adibi, 1979;Paxton and Harris, 1984a). In addition, clofibric acid has been reported to inhibit protein synthesis (Paul and Adibi, 1980).…”
Section: Introductionmentioning
confidence: 99%
“…We reported earlier that the treatments of intermediate MSUD patients with PB result in significantly lower circulating concentrations of BCAA and BCKA (20). Clofibric acid, which is derived from the anti-lipidemic drug clofibrate and functions as a weak BDK inhibitor (17), has also been used to lower BCAA concentration in rats (19,(24)(25)(26)(27). However, both PB and clofibric acid are significantly less potent BDK inhibitors (IC 50 of 53.1 and 812 μM, respectively), than (S)-CPP (IC 50 of 6.3 μM; Table 1).…”
Section: Discussionmentioning
confidence: 99%
“…Since the BCOD kinase gene is subject to tissue-specific regulation by glucocorticoids and nutritional stimuli, a similar mechanism may exist for regulating kinase gene expression in the liver. For example, clofibrate (p-chlorophenoxymethylpropionic acid), a well-known anti-hyperlipidaemic drug, was reported to increase hepatic BCOD-complex activity [43][44][45], which may be linked to the development of a muscular weakness syndrome after long-term treatment with the drug [46][47][48]. In a recent study [45], administration of clofibrate to chow-fed rats reduced the hepatic kinase mRNA and protein levels to 60 % and 30 % respectively of controls, which appeared to be responsible for the increased activity of the BCOD complex.…”
Section: Discussionmentioning
confidence: 99%