Low fatty acid elongation rate in the presence of NADH in the liver endoplasmic reticulum. Overinhibition by BSA at the beta-ketoreductase level.
The rate of NADH-dependent palmitoyl-CoA elongation was only 41% of that of NADH-dependent elongation in microsomes from rats fed a fat-free diet, in the absence of BSA. This value was markedly lowered to 5%, when the assay was performed in the presence of BSA. The determination of the intermediate products showed that 93% of the total products accumulated as beta-ketostearate in the presence of BSA and NADH, whereas the accumulated beta-ketostearate was only 25% of the total products in the presence of BSA and NADPH. BSA was shown to be responsible for the low rate of NADH-dependent elongation by inhibiting the beta-ketoreductase in the presence of NADH and, thereby, inducing beta-ketostearate accumulation. These results indicate that NADH is probably not the physiological electron donor to the elongation pathway.
Demirkapi
N
N
Institut National de la Santé et de la Recherche Médicale, U 56, Hôpital de Bicêtre, Le Kremlin-Bicêtre, France.
Ghesquier
D
D
D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000037:antagonists & inhibitors* / Q000378:metabolism; D000818:Animals; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D008297:Male; D008862:Microsomes, Liver / Q000378:metabolism* / Q000648:ultrastructure; D009243:NAD / Q000494:pharmacology*; D009249:NADP / Q000494:pharmacology; D010171:Palmitoyl Coenzyme A / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012710:Serum Albumin, Bovine / Q000494:pharmacology*; D013229:Stearic Acids / Q000378:metabolism*
D013229:Stearic Acids; D009243:NAD; C028241:16-ketostearic acid; D010171:Palmitoyl Coenzyme A; D012710:Serum Albumin, Bovine; D009249:NADP; D015094:3-Hydroxyacyl CoA Dehydrogenases