HIV-PROTEASE INHIBITORS INDUCE EXPRESSION OF SUPPRESSOR OF CYTOKINE SIGNALING-1

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 胰岛素抵抗、高血糖和2型糖尿病是代谢综合征的后遗症之一，60%-80%的人类免疫缺陷病毒(HIV)阳性患者接受HIV蛋白酶抑制剂(PI)治疗后会出现代谢综合征。然而，对于阐明导致这些变化的分子机制的研究(S)，主要集中在PI的急性体外作用上。在这里，我们研究了匹尼地那韦(IDV)对雄性Zucker糖尿病脂肪(FA/FA)(ZDF)大鼠的慢性(7wk)体内效应。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Insulin resistance, hyperglycemia, and type 2 diabetes are among the sequelae of metabolic syndromes that occur in 60-80% of human immunodeficiency virus (HIV)-positive patients treated with HIV-protease inhibitors (PIs). Studies to elucidate the molecular mechanism(s) contributing to these changes, however, have mainly focused on acute, in vitro actions of PIs. Here, we examined the chronic (7 wk) in vivo effects of the PI indinavir (IDV) in male Zucker diabetic fatty (fa/fa) (ZDF) rats.