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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Adiposity, dyslipidemia, and insulin resistance in mice with targeted deletion of phospholipid scramblase 3 (PLSCR3).
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Adiposity, dyslipidemia, and insulin resistance in mice with targeted deletion of phospholipid scramblase 3 (PLSCR3).

机译：有针对性地删除磷脂加扰酶3（PLSCR3）的小鼠的肥胖，血脂异常和胰岛素抵抗。

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摘要

The phospholipid scramblases (PLSCR1 to PLSCR4) are a structurally and functionally unique class of proteins, which are products of a tetrad of genes conserved from Caenorhabditis elegans to humans. The best characterized member of this family, PLSCR1, is implicated in the remodeling of the transbilayer distribution of plasma membrane phospholipids but is also required for normal signaling through select growth factor receptors. Mice with targeted deletion of PLSCR1 display perinatal granulocytopenia due to defective response of hematopoietic precursors to granulocyte colony-stimulating factor and stem cell factor. To gain insight into the biologic function of another member of the PLSCR family, we investigated mice with targeted deletion of PLSCR3, a protein that like PLSCR1 is expressed in many blood cells but which, by contrast to PLSCR1, is also highly expressed in fat and muscle. PLSCR3(-/-) mice at 2 months of age displayed aberrant accumulation of abdominal fat when maintained on standard rodentchow, which was accompanied by insulin resistance, glucose intolerance, and dyslipidemia. Primary adipocytes and cultured bone-marrow-derived macrophages from PLSCR3(-/-) mice were engorged with neutral lipid, and adipocytes displayed defective responses to exogenous insulin. Plasma of PLSCR3(-/-) mice was elevated in non-high-density lipoproteins, cholesterol, triglycerides, nonesterified fatty acids, and leptin, whereas adiponectin was low. These data suggest that the expression of PLSCR3 may be required for normal adipocyte and/or macrophage maturation or function and raise the possibility that deletions or mutations affecting the PLSCR3(-/-) gene locus may contribute to the risk for lipid-related disorders in humans.
机译：磷脂scramblases（PLSCR1至PLSCR4）是结构上和功能上独特的一类蛋白质，它们是秀丽隐杆线虫对人类保守的四联基因的产物。该家族中最有特色的成员PLSCR1与质膜磷脂的跨双分子层分布重塑有关，但通过选择的生长因子受体进行正常信号传递也是必需的。由于造血前体对粒细胞集落刺激因子和干细胞因子的缺陷应答，PLSCR1靶向缺失的小鼠表现出围产期粒细胞减少症。为了深入了解PLSCR家族另一个成员的生物学功能，我们研究了有针对性地缺失PLSCR3的小鼠。PLSCR3是一种蛋白质，其在许多血细胞中都表达，但与PLSCR1相比，它在脂肪和脂肪中也高表达。肌肉。当维持在标准啮齿动物上时，两个月大的PLSCR3（-/-）小鼠表现出腹部脂肪异常积累，并伴有胰岛素抵抗，葡萄糖耐受不良和血脂异常。 PLSCR3（-/-）小鼠的原代脂肪细胞和培养的源自骨髓的巨噬细胞充满中性脂质，并且脂肪细胞对外源胰岛素的反应不良。非高密度脂蛋白，胆固醇，甘油三酸酯，非酯化脂肪酸和瘦素中PLSCR3（-/-）小鼠的血浆升高，而脂联素则较低。这些数据表明，正常脂肪细胞和/或巨噬细胞的成熟或功能可能需要PLSCR3的表达，并增加了影响PLSCR3（-/-）基因位点的缺失或突变可能增加脂质相关疾病风险的可能性。人类。

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