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首页> 外文期刊>Journal of cellular physiology. >IPMK modulates hepatic glucose production and insulin signaling
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IPMK modulates hepatic glucose production and insulin signaling

机译：IPMK调节肝葡萄糖生产胰岛素信号传导

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摘要

Abstract Hepatic glucose production (HGP) is crucial for the maintenance of normal glucose homeostasis. Although hepatic insulin resistance contributes to excessive glucose production, its mechanism is not well understood. Here, we show that inositol polyphosphate multikinase (IPMK), a key enzyme in inositol polyphosphate biosynthesis, plays a role in regulating hepatic insulin signaling and gluconeogenesis both in vitro and in vivo. IPMK‐deficient hepatocytes exhibit decreased insulin‐induced activation of Akt‐FoxO1 signaling. The expression of messenger RNA levels of phosphoenolpyruvate carboxykinase 1 (Pck1) and glucose 6‐phosphatase (G6pc), key enzymes mediating gluconeogenesis, are increased in IPMK‐deficient hepatocytes compared to wild type hepatocytes. Importantly, re‐expressing IPMK restores insulin sensitivity and alleviates glucose production in IPMK‐deficient hepatocytes. Moreover, hepatocyte‐specific IPMK deletion exacerbates hyperglycemia and insulin sensitivity in mice fed a high‐fat diet, accompanied by an increase in HGP during pyruvate tolerance test and reduction in Akt phosphorylation in IPMK deficient liver. Our results demonstrate that IPMK mediates insulin signaling and gluconeogenesis and may be potentially targeted for treatment of diabetes.
机译：摘要肝葡萄糖生产(HGP)维护正常的葡萄糖的关键体内平衡。导致过多的葡萄糖生产,其机制还不是很清楚。,肌醇多磷酸盐multikinase (IPMK)肌醇多磷酸盐的关键酶生物合成,在调节肝脏中扮演了重要的角色胰岛素信号和糖质新生体外和体内。展览减少胰岛素诱导激活一种蛋白激酶FoxO1信号。RNA含量的磷酸烯醇丙酮酸carboxykinase 1地理(Pck1)和葡萄糖6磷酸酶(G6pc)键酶调节糖质新生,增加进入IPMK缺乏肝细胞而狂野肝细胞类型。恢复胰岛素敏感性和缓解葡萄糖生产IPMK缺乏肝细胞。此外,肝细胞地理IPMK删除加剧高血糖和胰岛素敏感性在高脂肪饮食的老鼠,伴随着一个丙酮酸耐受性测试期间增长最为迅猛并在IPMK减少一种蛋白激酶磷酸化有缺陷的肝脏。IPMK介导胰岛素信号和糖质新生和可能潜在的目标用于治疗糖尿病。

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