THE EFFECT OF LEPTIN THERAPY ON LIPID METABOLISM IN HIV-LIPODYSTROPHY

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 1.HIV脂肪营养不良综合征(HLS)与以下因素有关：a)全身脂肪代谢加速，总脂肪分解和净脂肪分解增加。B)脂肪酸氧化没有按比例增加。C)增加脂肪细胞内和肝脏内的再酯化。D)提高apoB-100的周转率。 2.HLS的瘦素治疗将刺激脂肪氧化，并将能量需求的燃料选择从碳水化合物转移到脂肪。脂肪分解释放的游离脂肪酸将从肝脏内的再酯化分流，VLDL apoB-100的合成转向氧化处理，从而改善高甘油三酯血症。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. 1. HIV Lipodystrophy Syndrome (HLS) is associated with: a) accelerated whole-body lipid kinetics with an increase in total and net lipolysis. b) absence of a proportional increase in fatty acid oxidation. c) increased intra- adipocyte and intra-hepatic re-esterification. d) increased turnover rate of apoB-100. 2. Leptin therapy in HLS will stimulate fat oxidation and shift fuel selection for energy requirements from carbohydrate to lipid. Free fatty acids released as a result of lipolysis will be shunted away from intra-hepatic re-esterification, and VLDL apoB-100 synthesis towards oxidative disposal, thus improving hypertriglyceridemia.