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首页> 外文期刊>Cell metabolism >Rescue of obesity-induced infertility in female mice due to a pituitary-specific knockout of the insulin receptor.
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Rescue of obesity-induced infertility in female mice due to a pituitary-specific knockout of the insulin receptor.

机译：由于胰岛素受体的垂体特异性敲除，在雌性小鼠中挽救肥胖引起的不育。

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Obesity is associated with insulin resistance in metabolic tissues such as adipose, liver, and muscle, but it is unclear whether nonclassical target tissues, such as those of the reproductive axis, are also insulin resistant. To determine if the reproductive axis maintains insulin sensitivity in obesity in vivo, murine models of diet-induced obesity (DIO) with and without intact insulin signaling in pituitary gonadotrophs were created. Diet-induced obese wild-type female mice (WT DIO) were infertile and experienced a robust increase in luteinizing hormone (LH) after gonadotropin-releasing hormone (GnRH) or insulin stimulation. By contrast, both lean and obese mice with a pituitary-specific knockout of the insulin receptor (PitIRKO) exhibited reproductive competency, indicating that insulin signaling in the pituitary is required for the reproductive impairment seen in DIO and that the gonadotroph maintains insulin sensitivity in a setting of peripheral insulin resistance.
机译：肥胖与新陈代谢组织（例如脂肪，肝脏和肌肉）中的胰岛素抵抗有关，但尚不清楚非经典靶组织（例如生殖轴组织）是否也具有胰岛素抵抗。为了确定在体内肥胖中生殖轴是否维持胰岛素敏感性，建立了在有和没有完整的垂体促性腺激素信号传导的饮食诱导的肥胖（DIO）小鼠模型。饮食诱导的肥胖野生型雌性小鼠（WT DIO）不育，促性腺激素释放激素（GnRH）或胰岛素刺激后，其促黄体生成激素（LH）呈强劲增加。相比之下，垂体特异性敲除胰岛素受体（PitIRKO）的瘦小鼠和肥胖小鼠均表现出生殖能力，这表明垂体中的胰岛素信号传导是DIO所见的生殖功能障碍所必需的，而促性腺激素可维持胰岛素敏感性周围胰岛素抵抗的设置。

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