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首页> 外文期刊>Endocrinology >The Absence of GH Signaling Affects the Susceptibility to High-Fat Diet-Induced Hypothalamic Inflammation in Male Mice
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The Absence of GH Signaling Affects the Susceptibility to High-Fat Diet-Induced Hypothalamic Inflammation in Male Mice

机译：GH信号的缺乏会影响高脂饮食诱发下丘脑炎症的雄性小鼠。

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GH is important in metabolic control, and mice with disruption of the gene encoding the GH receptor (GHR) and GH binding protein (GHR-/- mice) are dwarf with low serum IGF-1 and insulin levels, high GH levels, and increased longevity, despite their obesity and altered lipid and metabolic profiles. Secondary complications of high-fat diet (HFD)-induced obesity are reported to be associated with hypothalamic inflammation and gliosis. Because GH and IGF-1 can modulate inflammatory processes, our objective was to evaluate the effect of HFD on hypothalamic inflammation/gliosis in the absence of GH signaling and determine how this correlates with changes in systemic metabolism. On normal chow, GHR-/- mice had a higher percentage of fat mass and increased circulating nonesterified free fatty acids levels compared with wild type (WT), and this was associated with increased hypothalamic TNF-alpha and phospho-JNK levels. After 7 weeks on a HFD, both WT and GHR-/- mice had increased weight gain, with GHR-/- mice having a greater rise in their percentage of body fat. InWT mice, HFD-induced weight gain was associated with increased hypothalamic levels of phospho-JNK and the microglial marker Iba-1 (ionized calcium-binding adapter molecule 1) but decreased cytokine production. Moreover, in GHR-/- mice, the HFD decreased hypothalamic inflammatory markers to WT levels with no indication of gliosis. Thus, the GH/IGF-1 axis is important in determining not only adipose tissue accrual but also the inflammatory response to HFD. However, how hypothalamic inflammation/gliosis is defined will determine whether it can be considered a common feature of HFD induced obesity.
机译：GH在代谢控制中很重要，而编码GH受体（GHR）和GH结合蛋白的基因被破坏的小鼠（GHR-/-小鼠）较矮，血清IGF-1和胰岛素水平低，GH水平高，且增加尽管他们肥胖，并且脂质和代谢状况发生了改变，但仍能长寿。据报道，高脂饮食（HFD）引起的肥胖症的继发并发症与下丘脑炎症和神经胶质增生有关。因为GH和IGF-1可以调节炎症过程，所以我们的目标是评估在没有GH信号的情况下HFD对下丘脑炎症/神经胶质增生的影响，并确定其与全身代谢变化之间的关系。与野生型（WT）相比，正常饮食的GHR-/-小鼠脂肪含量更高，循环非酯化游离脂肪酸水平更高，这与下丘脑TNF-α和磷酸JNK水平升高有关。在HFD上7周后，WT和GHR-/-小鼠的体重增加均增加，而GHR-/-小鼠的体脂百分比增加更大。在野生型小鼠中，HFD诱导的体重增加与下丘脑水平的磷酸JNK和小胶质标记物Iba-1（离子钙结合适配器分子1）增加有关，但细胞因子产生减少。此外，在GHR-/-小鼠中，HFD将下丘脑炎症标志物降低至WT水平，而没有神经胶质增生的迹象。因此，GH / IGF-1轴不仅在确定脂肪组织的累积，而且在确定对HFD的炎症反应中都非常重要。然而，下丘脑炎症/神经胶质细胞增生的定义将决定是否可以将其视为HFD诱发肥胖的共同特征。

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