Ohsumi J, Sakakibara S, Yamaguchi J, Miyadai K, Yoshioka S, Fujiwara T, Horikoshi H, Serizawa N
Biomedical Research Laboratories, Sankyo Co. Ltd., Tokyo, Japan.
Endocrinology. 1994 Nov;135(5):2279-82. doi: 10.1210/endo.135.5.7956951.
Tumor necrosis factor (TNF) is implicated in wasting syndromes and insulin resistance in chronic infection and obese-linked diabetes. TNF (10 ng/ml) inhibited adipocyte differentiation of 3T3-L1 cells, and in these TNF treated cells little insulin-stimulated glucose uptake was observed. Treatment of 3T3-L1 cells with troglitazone (1-10 microM) partially prevented this inhibitory effect of TNF on adipogenesis, and enhanced expression of C/EBP alpha and GLUT4, even in the presence of TNF. Troglitazone also prevented the inhibitory effects of interleukin-1, interleukin-6, and leukemia inhibitory factor, but not of transforming growth factor beta on adipocyte differentiation of 3T3-L1 cells. These effects might contribute to the antidiabetic effect of troglitazone in obese diabetic animals.
肿瘤坏死因子（TNF）与慢性感染和肥胖相关糖尿病中的消瘦综合征及胰岛素抵抗有关。TNF（10纳克/毫升）抑制3T3-L1细胞的脂肪细胞分化，并且在这些经TNF处理的细胞中几乎未观察到胰岛素刺激的葡萄糖摄取。用曲格列酮（1-10微摩尔）处理3T3-L1细胞可部分阻止TNF对脂肪生成的这种抑制作用，并且即使在存在TNF的情况下也能增强C/EBPα和GLUT4的表达。曲格列酮还可阻止白细胞介素-1、白细胞介素-6和白血病抑制因子的抑制作用，但不能阻止转化生长因子β对3T3-L1细胞脂肪细胞分化的抑制作用。这些作用可能有助于曲格列酮在肥胖糖尿病动物中的抗糖尿病作用。
