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首页> 外文期刊>Molecular and Cellular Biology >Lipocalin-13 Regulates Glucose Metabolism by both Insulin-Dependent and Insulin-Independent Mechanisms
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Lipocalin-13 Regulates Glucose Metabolism by both Insulin-Dependent and Insulin-Independent Mechanisms

机译：Lipocalin-13通过胰岛素依赖性和胰岛素依赖性机制调节葡萄糖代谢。

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Insulin sensitivity is impaired in obesity, and insulin resistance is the primary risk factor for type 2 diabetes. Here we show that lipocalin-13 (LCN13), a lipocalin superfamily member, is a novel insulin sensitizer. LCN13 was secreted by multiple cell types. Circulating LCN13 was markedly reduced in mice with obesity and type 2 diabetes. Three distinct approaches were used to increase LCN13 levels: LCN13 transgenic mice, LCN13 adenoviral infection, and recombinant LCN13 administration. Restoration of LCN13 significantly ameliorated hyperglycemia, insulin resistance, and glucose intolerance in mice with obesity. LCN13 enhanced insulin signaling not only in animals but also in cultured adipocytes. Recombinant LCN13 increased the ability of insulin to stimulate glucose uptake in adipocytes and to suppress hepatic glucose production (HGP) in primary hepatocyte cultures. Additionally, LCN13 alone was able to suppress HGP, whereas neutralization of LCN13 increased HGP in primary hepatocyte cultures. These data suggest that LCN13 regulates glucose metabolism by both insulin-dependent and insulin-independent mechanisms. LCN13 and LCN13-related molecules may be used to treat insulin resistance and type 2 diabetes.
机译：肥胖会损害胰岛素敏感性，而胰岛素抵抗是2型糖尿病的主要危险因素。在这里，我们显示lipocalin-13（LCN13），lipocalin超家族成员，是一种新型的胰岛素敏化剂。 LCN13由多种细胞类型分泌。肥胖和2型糖尿病小鼠的循环LCN13明显减少。三种不同的方法用于提高LCN13的水平： LCN13 转基因小鼠，LCN13腺病毒感染和重组LCN13施用。 LCN13的恢复显着改善了肥胖小鼠的高血糖，胰岛素抵抗和葡萄糖耐受不良。 LCN13不仅在动物中而且在培养的脂肪细胞中都增强胰岛素信号传导。重组LCN13增加了胰岛素刺激脂肪细胞摄取葡萄糖并抑制原代肝细胞培养物中肝葡萄糖生成（HGP）的能力。此外，单独的LCN13能够抑制HGP，而中和LCN13可增加原代肝细胞培养物中的HGP。这些数据表明，LCN13通过胰岛素依赖性和胰岛素依赖性机制调节葡萄糖代谢。 LCN13和LCN13相关分子可用于治疗胰岛素抵抗和2型糖尿病。

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