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

HIV 蛋白酶抑制剂诱导细胞因子信号传导抑制子 1 的表达

• 批准号: 7953996
• 负责人: Michael J Carper
• 金额: $ 0.58万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-02-01 至 2010-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7953996
• 关键词: Acute; Chronic; Computer Retrieval of Information on Scientific Projects Database; Cytokine Inducible SH2-Containing Protein; Funding; Grant; HIV; HIV Protease Inhibitors; Hyperglycemia; In Vitro; Indinavir; Institution; Insulin Resistance; Mass Spectrum Analysis; Metabolic syndrome; Molecular; Non-Insulin-Dependent Diabetes Mellitus; Patients; Protease Inhibitor; Rattus; Research; Research Personnel; Resources; Source; United States National Institutes of Health; biomedical resource; diabetic; in vivo; male

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.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 胰岛素抵抗、高血糖症和2型糖尿病是代谢综合征的后遗症，60-80%接受艾滋病毒蛋白酶抑制剂（PI）治疗的人类免疫缺陷病毒（HIV）阳性患者都会出现这些后遗症。然而，阐明这些变化的分子机制的研究主要集中在PI的急性体外作用上。在这里，我们研究了慢性（7周）在雄性Zucker糖尿病脂肪（fa/fa）（ZDF）大鼠体内的PI茚地那韦（IDV）的影响。