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首页> 外文期刊>Biochimica et Biophysica Acta. Molecular and cell biology of Lipids >Role of hepatic lipase and scavenger receptor BI in clearing phospholipid/free cholesterol-rich lipoproteins in PLTP-deficient mice
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Role of hepatic lipase and scavenger receptor BI in clearing phospholipid/free cholesterol-rich lipoproteins in PLTP-deficient mice

机译：肝脂肪酶和清除剂受体BI在清除PLTP缺陷小鼠的磷脂/游离富含胆固醇的脂蛋白中的作用

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Phospholipid transfer protein knock-out (PLTP0) mice have defective transfer of phospholipids (PL) from triglyceride-rich lipoproteins (TRL) into high-density lipoproteins (HDL). In this study, we examined the role of diet, hepatic lipase (HL) and scavenger receptor BI (SRBI) in determining the accumulation of excess PL and free cholesterol (FC, "surface remnants") in plasma of PLTP0 mice. PL and FC accumulated in the very low-density lipoprotein (VLDL)-LDL region of PLTP0 mice on a highly saturated, coconut oil-based diet, but not on chow or milk-fat based Western diets. Accumulation of PL and FC was dramatically increased in PLTP0/HL0 mice, compared to PLTP0 mice, but only on the coconut oil diet. Turnover studies indicated that the coconut oil diet was associated with delayed catabolism of PL of PL/FC-rich particles. Incubation of these particles with primary hepatocytes in the presence of SRBI neutralizing antibody indicated that SRBI was primarily responsible for removal of FC and PL on the Western diet. In hepatocytes of coconut oil-fed mice, removal of FC and PL from these particles by SRBI was markedly reduced, even though SRBI protein expression levels were unchanged. These studies indicate that HL and SRBI both have major role in the clearance of PL and FC of surface remnants in PLTP0 micr. SRBI appears to be dysfunctional in coconut oil diet-fed animals, possibly related to changes in hepatocyte membrane fatty acid composition.
机译：磷脂转运蛋白敲除（PLTP0）小鼠的磷脂（PL）从富含甘油三酸酯的脂蛋白（TRL）到高密度脂蛋白（HDL）的转移有缺陷。在这项研究中，我们检查了饮食，肝脂肪酶（HL）和清除剂受体BI（SRBI）在确定PLTP0小鼠血浆中过量PL和游离胆固醇（FC，“表面残留物”）的积累中的作用。在高度饱和的，以椰子油为基础的饮食中，PLTP0小鼠的极低密度脂蛋白（VLDL）-LDL区域中会积累PL和FC，而在以杂粮或乳脂为基础的西方饮食中，则不会。与PLTP0小鼠相比，PLTP0 / HL0小鼠中PL和FC的积累显着增加，但仅在椰子油饮食中。营业额研究表明，椰子油饮食与富含PL / FC的PL的PL分解代谢延迟有关。在SRBI中和抗体的存在下，这些颗粒与原代肝细胞一起温育表明SRBI主要负责去除西方饮食中的FC和PL。在用椰子油喂养的小鼠的肝细胞中，即使SRBI蛋白表达水平没有变化，通过SRBI从这些颗粒中去除FC和PL的情况仍显着减少。这些研究表明，HL和SRBI都在清除PLTP0胶中表面残留物的PL和FC中起主要作用。 SRBI在以椰子油为食的动物中似乎功能失调，可能与肝细胞膜脂肪酸组成的变化有关。

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