Iida N, Iida R, Takeyama N, Tanaka T
Department of Emergency and Critical Care Medicine, Kansai Medical University, Osaka, Japan.
Biochem Mol Biol Int. 1993 May;30(1):177-85.
The effects of diabetes on fatty acid oxidation in platelets was determined in streptozotocin-induced diabetic rats. In platelets isolated from diabetes, the oxygen consumption which reflects mainly the degree of fatty acid oxidation and ADP- and thrombin-induced aggregation were increased as compared to non-diabetic rat platelets. Carnitine palmitoyltransferase I (CPT I), the rate-limiting enzyme for fatty acid oxidation, in platelets obtained from diabetes showed a higher Vmax for palmitoyl-CoA and an increased I50 (concentration giving 50% inhibition of CPT I activity) for malonyl-CoA inhibition. These changes observed in fatty acid oxidation in platelets derived from diabetes returned to the control levels after insulin therapy. When platelets were stimulated with thrombin, platelet CPT I activity increased over time in both diabetic and non-diabetic rats. From these findings, fatty acid oxidation in platelets, as in the liver, is likely to be regulated by insulin and both increased CPT I activity and decreased sensitivity to malonyl-CoA inhibition are attributable to enhanced platelet fatty acid oxidation in diabetic rats.
在链脲佐菌素诱导的糖尿病大鼠中，测定了糖尿病对血小板脂肪酸氧化的影响。与非糖尿病大鼠血小板相比，从糖尿病大鼠分离的血小板中，主要反映脂肪酸氧化程度的耗氧量以及二磷酸腺苷（ADP）和凝血酶诱导的聚集均增加。肉碱棕榈酰转移酶I（CPT I）是脂肪酸氧化的限速酶，糖尿病大鼠血小板中的CPT I对棕榈酰辅酶A表现出更高的最大反应速度（Vmax），对丙二酰辅酶A抑制的半数抑制浓度（I50）增加。糖尿病大鼠血小板中观察到的这些脂肪酸氧化变化在胰岛素治疗后恢复到对照水平。当用凝血酶刺激血小板时，糖尿病和非糖尿病大鼠血小板中的CPT I活性均随时间增加。从这些发现来看，血小板中的脂肪酸氧化与肝脏一样，可能受胰岛素调节，CPT I活性增加和对丙二酰辅酶A抑制的敏感性降低均归因于糖尿病大鼠血小板脂肪酸氧化增强。
