Olubadewo J O, Heimberg M
Biochem Biophys Res Commun. 1985 Nov 15;132(3):1001-7. doi: 10.1016/0006-291x(85)91906-0.
Hepatocytes from T3-treated rats synthesized less triglyceride and more ketone bodies from [1-14C]oleate at all concentrations from 0-2 mM, than did hepatocytes from euthyroid animals; addition of 1.0 mM glycerol increased triglyceride synthesis and reduced ketogenesis in hepatocytes from T3-treated rats to the rates observed in euthyroid hepatocytes in the absence of added glycerol. Glycerol did not alter triglyceride synthesis, but reduced ketogenesis genesis by euthyroid hepatocytes. It is probable from these and other data (J. Biol. Chem. 259, 8857-8862 (1985)) that, in the hyperthyroid rat, glycero-3-P, and not fatty acid, is rate limiting for synthesis of triglyceride, and, secondarily for reducing rates of ketogenesis in the hepatocyte.
在0至2 mM的所有浓度下,与甲状腺功能正常动物的肝细胞相比,用T3处理的大鼠的肝细胞从[1-14C]油酸合成的甘油三酯更少,酮体更多;添加1.0 mM甘油可增加用T3处理的大鼠肝细胞中的甘油三酯合成,并将生酮作用降低至在未添加甘油的情况下甲状腺功能正常的肝细胞中观察到的速率。甘油不会改变甲状腺功能正常的肝细胞的甘油三酯合成,但会降低其生酮作用。根据这些以及其他数据(《生物化学杂志》259, 8857 - 8862 (1985)),在甲状腺功能亢进的大鼠中,甘油-3-磷酸而非脂肪酸是甘油三酯合成的限速因素,其次是降低肝细胞中生酮作用的速率。