Wentworth J M, Burris T P, Chatterjee V K
Level 5, Department of Medicine, Addenbrookes, Cambridge CB2 2QQ, UK.
J Endocrinol. 2000 Feb;164(2):R7-R10. doi: 10.1677/joe.0.164r007.
A recent prospective clinical study has shown that antiviral therapy with HIV protease inhibitors (PIs) is associated with a syndrome of peripheral fat wasting (lipodystrophy) and disordered glucose and lipid metabolism (Carr et al. 1999). We have studied the effects of indinavir and saquinavir, two HIV protease inhibitors, on cultured primary human preadipocytes and report that these compounds inhibit their differentiation. However, we find that these agents do not inhibit either transcriptional activation or adipocyte P2 gene induction by the PPARgamma/RXR nuclear receptor heterodimer. Together, our findings suggest that impaired adipogenesis is the basis of PI-associated lipodystrophy, but that this occurs via a PPARgamma/RXR-independent mechanism.
最近一项前瞻性临床研究表明,使用HIV蛋白酶抑制剂(PIs)进行抗病毒治疗与外周脂肪消耗综合征(脂肪代谢障碍)以及糖脂代谢紊乱有关(卡尔等人,1999年)。我们研究了两种HIV蛋白酶抑制剂茚地那韦和沙奎那韦对培养的原代人前脂肪细胞的影响,并报告这些化合物会抑制其分化。然而,我们发现这些药物既不抑制PPARγ/RXR核受体异二聚体的转录激活,也不抑制脂肪细胞P2基因的诱导。我们的研究结果共同表明,脂肪生成受损是PI相关脂肪代谢障碍的基础,但这是通过一种不依赖PPARγ/RXR的机制发生的。