Hormonal and Developmental Factors Affecting Carnitine Palmitoyltransferase (1) and (2) Activities in Rat Liver

概要

論文の詳細を見る
Mitochondrial inner-membrane is impermeable to acyl CoA. Thus, for a fatty acid to be oxidized, this step is bypassed via palmitylcarnitine which readily reaches β-oxidation site1). In order to fulfil its role, carnitine palmitoyltransferase (CPT) has to be present at both outside and inside the permeable barrier of the innermembrane. Indeed, it has been lately shown that CPT is present as isozymes2). One is loosely bound to outside of the inner-membrane and is inhibited by bromoacy 1CoA in the presence of carnitine (CPT 1). The other form is firmly bound to the mitochondrial inner-membrane and is not inhibited by the above mentioned inhibitor (CPT 2)3, 4). Therefore, in this study, in order to identify the possible regulatory role of CPT (1) and (2) enzymes in fatty acid oxidation, CPT (1) and (2) activities were measured in liver mitochondria from diabetic, fetal and neonatal rats. Under these conditions, hepatic fatty acid oxidation has been reported to be either enhanced or diminished5, 6). A simplified new method has been developed to measure both CPT (1) and (2) activities by using DTNB. An effect of glucagon in the developing rat on liver CPT activities was also studied. In rat liver mitochondria, palmitate was oxidized by either carnitine-independent or dependent pathway. However, the former capacity is about one fourth of the latter indicating the predominat role of carnitine-depenent pathway. In liver mitochondria from diabetic rats, both of the pathways were stimulated. Regarding carnitine-depdndent pathway, both CPT (1) and (2) activities were elevated by 50-70% in liver mitochondria from diabetic rats. Insulin treatment reversed these increases. In fetal rat liver, aftty acid oxidation as well as CPT (1) activity remained low, but within 2-3 days after birth, 3 to 5- fold elevation was found. CPT (2) activity preceded these increases in the late fetal life (20-21 days gestation). Glucagon injection to the fetases of 21 days gestation induced CPT (1) activity after five hours. These results indicate that CPT (1) activity is a rate-controlling step for longchain fatty acid oxidation in the liver and is under hormonal control especially by insulin. The appearance of hepatic fatty acid oxidation in the neonatal rat paralleled to that of CPT (1), but not of CPT (2) activity. The development of CPT (1) activity may be an induction mediated by cyclic AMP.

Hormonal and Developmental Factors Affecting Carnitine Palmitoyltransferase (1) and (2) Activities in Rat Liver

スポンサーリンク

概要

著者

関連論文

スポンサーリンク