Grunfeld C, Pang M, Doerrler W, Shigenaga J K, Jensen P, Feingold K R
Department of Medicine, University of California, San Francisco.
J Clin Endocrinol Metab. 1992 May;74(5):1045-52. doi: 10.1210/jcem.74.5.1373735.
Infection causes disturbances in lipid metabolism that may be mediated by cytokines. Therefore we studied plasma lipids, lipoproteins, triglyceride (TG) metabolism, and serum cytokines in three groups: patients with the acquired immunodeficiency syndrome (AIDS) without active secondary infection, patients with evidence of human immunodeficiency virus infection but without clinical AIDS (HIV+), and controls. Plasma TGs and FFA were increased in AIDS, while plasma cholesterol, high density lipoprotein (HDL) cholesterol, apolipoprotein-A-1 (Apo-A-1), low density lipoprotein (LDL) cholesterol, and Apo-B-100 levels were decreased. Increased TG levels in AIDS were primarily due to increases in very low density lipoprotein of normal composition; in addition, LDL and HDL were TG enriched. In HIV+, TGs and FFA were not increased, but total cholesterol, HDL cholesterol, Apo-A-1, and Apo-B-100 were significantly decreased. Interferon-alpha (IFN alpha) and C-reactive protein levels were increased in AIDS, but tumor necrosis factor and haptoglobin levels were not. There was a significant correlation between plasma TGs and IFN alpha levels (r = 0.477; P less than 0.01), but not between TGs and tumor necrosis factor, C-reactive protein, haptoglobin, or P-24 antigen. In addition, there was no relationship between circulating IFN alpha levels and plasma cholesterol, HDL cholesterol, Apo-A-1, LDL cholesterol, Apo-B-100, or FFA. TG clearance time and postheparin lipase were significantly decreased in AIDS and HIV+. There was a strong correlation between serum IFN alpha levels and TG clearance time in AIDS and HIV+ (r = 0.783; P less than 0.001). In summary, decreases in cholesterol and cholesterol containing lipoproteins (including HDL) in both AIDS and HIV+ precede the appearance of hypertriglyceridemia and are not related to IFN alpha or TG levels. Our data raise the possibility that with development of AIDS, subsequent increases in IFN alpha may contribute to increases in plasma TG levels in part by decreasing the clearance of TG.
感染会引发脂质代谢紊乱，这种紊乱可能由细胞因子介导。因此，我们研究了三组人群的血浆脂质、脂蛋白、甘油三酯（TG）代谢及血清细胞因子：无活动性继发感染的获得性免疫缺陷综合征（AIDS）患者、有人类免疫缺陷病毒感染证据但无临床AIDS的患者（HIV+）以及对照组。AIDS患者的血浆TG和游离脂肪酸（FFA）升高，而血浆胆固醇、高密度脂蛋白（HDL）胆固醇、载脂蛋白A-1（Apo-A-1）、低密度脂蛋白（LDL）胆固醇及Apo-B-100水平降低。AIDS患者TG水平升高主要归因于正常组成的极低密度脂蛋白增加；此外，LDL和HDL富含TG。在HIV+患者中，TG和FFA未升高，但总胆固醇、HDL胆固醇、Apo-A-1及Apo-B-100显著降低。AIDS患者的干扰素-α（IFNα）和C反应蛋白水平升高，但肿瘤坏死因子和触珠蛋白水平未升高。血浆TG与IFNα水平之间存在显著相关性（r = 0.477；P＜0.01），但TG与肿瘤坏死因子、C反应蛋白、触珠蛋白或P-24抗原之间无相关性。此外，循环IFNα水平与血浆胆固醇、HDL胆固醇、Apo-A-1、LDL胆固醇、Apo-B-100或FFA之间无关联。AIDS和HIV+患者的TG清除时间及肝素后脂肪酶显著降低。AIDS和HIV+患者的血清IFNα水平与TG清除时间之间存在强相关性（r = 0.783；P＜0.001）。总之，AIDS和HIV+患者中胆固醇及含胆固醇脂蛋白（包括HDL）的降低先于高甘油三酯血症出现，且与IFNα或TG水平无关。我们的数据提示，随着AIDS的发展，随后IFNα的增加可能部分通过降低TG清除率而导致血浆TG水平升高。
