Elayan I M, Cartmill D C, Eckersell C B, Wilkin J, Winder W W
Department of Zoology, Brigham Young University, Provo, Utah 84602.
Proc Soc Exp Biol Med. 1991 Oct;198(1):569-71. doi: 10.3181/00379727-198-43290.
Malonyl-CoA, the inhibitor of carnitine palmitoyl transferase I, has been examined in this study in the muscle and liver of diabetic rats. Male Sprague-Dawley rats were rendered diabetic with streptozotocin (6 mg/100 g body wt). The gastrocnemius/plantaris muscles and liver samples were frozen at liquid nitrogen temperature. Muscle malonyl-CoA was 1.8 +/- 0.2 pmol/mg in control rats and 1.5 +/- 0.2 pmol/mg in the diabetic rats. This difference was not statistically significant. Liver malonyl-CoA of control rats was 8.6 +/- 0.8 pmol/mg, in comparison to 4.3 +/- 0.6 pmol/mg in diabetic rats. In the liver, high concentrations of malonyl-CoA inhibit fatty acid oxidation and ketogenesis. Failure of malonyl-CoA to decline in muscle in the diabetic may be responsible in part for the diversion of fatty acids to the liver, thereby enhancing hepatic fatty acid oxidation and ketogenesis.
本研究在糖尿病大鼠的肌肉和肝脏中检测了肉碱棕榈酰转移酶I的抑制剂丙二酰辅酶A。将雄性Sprague-Dawley大鼠用链脲佐菌素(6毫克/100克体重)诱导成糖尿病模型。腓肠肌/跖肌和肝脏样本在液氮温度下冷冻。对照组大鼠肌肉中的丙二酰辅酶A为1.8±0.2皮摩尔/毫克,糖尿病大鼠为1.5±0.2皮摩尔/毫克。这种差异无统计学意义。对照组大鼠肝脏中的丙二酰辅酶A为8.6±0.8皮摩尔/毫克,而糖尿病大鼠为4.3±0.6皮摩尔/毫克。在肝脏中,高浓度的丙二酰辅酶A会抑制脂肪酸氧化和酮体生成。糖尿病大鼠肌肉中丙二酰辅酶A未能下降,这可能部分导致脂肪酸转向肝脏,从而增强肝脏脂肪酸氧化和酮体生成。