Hülsmann W C, Dubelaar M L
Department of Biochemistry I, Medical Faculty, Erasmus University, Rotterdam, The Netherlands.
Mol Cell Biochem. 1988 Feb;79(2):147-51. doi: 10.1007/BF02424557.
Tumor Necrosis Factor (TNF) inhibits lipoprotein lipase activity in cultured myocytes and in the Langendorff rat heart after 3 h perfusion with TNF of glucocorticoid-pretreated rats. TNF acutely stimulates glyc(ogen)olysis and concomitantly endogenous lipolysis. The latter was significantly increased only when rats had been pretreated with glucocorticoid or fed a trierucate-rich diet. Under these conditions, contractile activity of the Langendorff hearts was acutely increased by TNF. The mechanism of the acute increase of contractile function and the accompanying increased glycolytic and lipolytic activities, by TNF, may be explained by increased cytosolic Ca2+ and cAMP levels.
肿瘤坏死因子(TNF)在对糖皮质激素预处理的大鼠灌注TNF 3小时后,可抑制培养的心肌细胞和Langendorff大鼠心脏中的脂蛋白脂肪酶活性。TNF可急性刺激糖原分解,并同时刺激内源性脂肪分解。仅当大鼠用糖皮质激素预处理或喂食富含三油精酸甘油酯的饮食时,后者才会显著增加。在这些条件下,TNF可使Langendorff心脏的收缩活性急性增加。TNF引起的收缩功能急性增加以及伴随的糖酵解和脂肪分解活性增加的机制,可能是由于细胞溶质Ca2+和cAMP水平升高所致。