The mechanism for the hypercholesterolemia induced by amino acids

本文探讨了过量组氨酸引起大鼠高胆固醇血症的机制。肝脏中的体内胆固醇生成增加。组氨酸过量饮食组大鼠肝脏HMG-CoA还原酶的活性和总活性均显著升高。此外，肝脏中的HMG-CoA还原酶mRNA也升高。然而，肝胆固醇7 α-羟化酶是胆固醇降解的限速酶，不受组氨酸过量饮食的影响。因此，肝脏中胆固醇合成增加可能是导致高胆固醇血症的原因。因此，皮质酮升高可能诱发高胆固醇血症。

The mechanism for the hypercholesterolemia induced by excess dietary histidine was investigated in rats. The in vivo cholesterogenesis in the liver increased. Both the active and total activities of liver HMG-CoA reductase that is rate limiting step were significantly increased when rats were fed the histidine-excess diet. Furthermore, HMG-CoA reductase mRNA in the liver was also elevated. Whereas, hepatic cholesterol 7alpha-hydroxylase which is the rate limiting for the cholesterol degradation was not affected by the histidine-excess diet. Thus, the increased synthesis of cholesterol in the liver might be responsible for the hypercholesterolemia.Feeding of the histidine-excess diet caused the stimulation in the corticosterone in the serum. Therefore, the increased corticosterone might induce the hypercholesterolemia.