Lee K H, White K J, Robinson J P, Kim K H
Department of Biochemistry, Purdue University, West Lafayette, Indiana 47907.
Mol Endocrinol. 1990 Nov;4(11):1671-8. doi: 10.1210/mend-4-11-1671.
Tumor necrosis factor/cachectin (TNF) inhibits differentiation of 30A5 preadipocytes into adipocytes. In this process, TNF inhibits the expression of the gene for acetyl-coenzyme-A carboxylase, the rate-limiting enzyme for biogenesis of long chain fatty acids. One of the early reactions caused by TNF is the Ca2+ redistribution of Ca2+ from the bound form to the free form. This Ca2+ redistribution results in a transient Ca2+ efflux. High concentrations of Mg2+ inhibit Ca2+ redistribution and efflux. This inhibition reverses the repression of acetyl-coenzyme-A carboxylase and reverses the TNF inhibition of the differentiation of 30A5 preadipocytes into adipocytes. This indicates that Ca2+ redistribution between the bound and the free form is an obligatory event in the sequence of actions caused by TNF in 30A5 cells.
肿瘤坏死因子/恶病质素（TNF）抑制30A5前脂肪细胞向脂肪细胞的分化。在此过程中，TNF抑制乙酰辅酶A羧化酶基因的表达，乙酰辅酶A羧化酶是长链脂肪酸生物合成的限速酶。TNF引起的早期反应之一是Ca2+从结合形式重新分布到游离形式。这种Ca2+重新分布导致短暂的Ca2+外流。高浓度的Mg2+抑制Ca2+重新分布和外流。这种抑制作用逆转了乙酰辅酶A羧化酶的抑制，并逆转了TNF对30A5前脂肪细胞向脂肪细胞分化的抑制。这表明结合形式和游离形式之间的Ca2+重新分布是TNF在30A5细胞中引起的一系列作用中的一个必要事件。
