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首页> 外文期刊>American Journal of Physiology >Remodeling of the HDL in NIDDM: a fundamental role for cholesteryl ester transfer protein.
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Remodeling of the HDL in NIDDM: a fundamental role for cholesteryl ester transfer protein.

机译：NIDDM中HDL的重塑：胆固醇酯转移蛋白的基本作用。

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摘要

When the Ay gene is expressed in KK mice, the yellow offspring (KKAy mice) become obese, insulin resistant, hyperglycemic, and severely hypertriglyceridemic, yet they maintain extraordinarily high plasma high-density lipoprotein (HDL) levels. Mice lack the ability to redistribute neutral lipids among circulating lipoproteins, a process catalyzed in humans by cholesteryl ester transfer protein (CETP). To test the hypothesis that it is the absence of CETP that allows these hypertriglyceridemic mice to maintain high plasma HDL levels, simian CETP was expressed in the KKAy mouse. The KKAy-CETP mice retained the principal characteristics of KKAy mice except that their plasma HDL levels were reduced (from 159 +/- 25 to 25 +/- 6 mg/dl) and their free apolipoprotein A-I concentrations increased (from 7 +/- 3 to 22 +/- 6 mg/dl). These changes appeared to result from a CETP-induced enrichment of the HDL with triglyceride (from 6 +/- 2 to 60 +/- 18 mol of triglyceride/mol of HDL), an alteration that renders HDL susceptible to destruction by lipases. These data support the premise that CETP-mediated remodeling of the HDL is responsible for the low levels of that lipoprotein that accompany hypertriglyceridemic non-insulin-dependent diabetes mellitus.
机译：当Ay基因在KK小鼠中表达时，黄色后代（KKAy小鼠）变得肥胖，胰岛素抵抗，高血糖和严重高甘油三酸酯血症，但它们却保持了极高的血浆高密度脂蛋白（HDL）水平。小鼠缺乏在循环脂蛋白之间重新分配中性脂质的能力，胆固醇脂蛋白转移蛋白（CETP）在人体内催化了这一过程。为了检验以下假设：缺少CETP可使这些高甘油三酸酯血症的小鼠维持较高的血浆HDL水平，在KKAy小鼠中表达了猿猴CETP。 KKAy-CETP小鼠保留了KKAy小鼠的主要特征，除了血浆HDL水平降低（从159 +/- 25降至25 +/- 6 mg / dl）和游离载脂蛋白AI浓度增加（从7 +/-） 3至22 +/- 6 mg / dl）。这些变化似乎是由CETP诱导的HDL富含甘油三酸酯（从6 +/- 2到60 +/- 18 mol甘油三酸酯/ mol HDL）引起的，这种改变使HDL易于被脂肪酶破坏。这些数据支持以下前提：CETP介导的HDL重塑是导致高甘油三酯血症非胰岛素依赖型糖尿病伴有的脂蛋白水平低的原因。

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