MNK1 and MNK2 mediate adverse effects of high-fat feeding in distinct ways.
MNK1 and MNK2 mediate adverse effects of high-fat feeding in distinct ways.
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MNK1 和 MNK2 以不同的方式介导高脂肪喂养的不利影响
DOI：
10.1038/srep23476
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发表时间：
2016-04-18
影响因子：
4.6
通讯作者：
Proud CG
中科院分区：
文献类型：
--
作者：
Moore CE;Pickford J;Cagampang FR;Stead RL;Tian S;Zhao X;Tang X;Byrne CD;Proud CG
MAP激酶相互作用激酶（MNK1和MNK2）是由MAP激酶激活的非必需酶。它们与控制蛋白质合成有关。在这里，我们展示了MNK1或MNK2表达被敲除（KO）的小鼠可以以不同的方式免受高脂肪喂养的不利影响。高脂肪饮食（HFD）喂养的MNK2-KO与野生型动物相比，体重增加较少，葡萄糖耐量改善，胰岛素敏感性改善，脂肪组织炎症明显减轻。这表明MNK2在脂肪形成和/或脂肪形成以及巨噬细胞生物学中发挥作用。MNK1-KO/HFD小鼠表现出更好的葡萄糖耐量和胰岛素敏感性，但体重增加，并表现出与WT动物相似的脂肪炎症。这些数据表明MNK1参与介导hfd诱导的胰岛素抵抗。我们的研究结果揭示了mnk在疾病生物学的新领域代谢功能障碍中的独特作用，并表明它们是管理代谢疾病的潜在新靶点。
The MAP kinase-interacting kinases (MNK1 and MNK2) are non-essential enzymes which are activated by MAP kinases. They are implicated in controlling protein synthesis. Here we show that mice in which the expression of either MNK1 or MNK2 has been knocked out (KO) are protected against adverse effects of high-fat feeding, and in distinct ways. High-fat diet (HFD)-fed MNK2-KO show less weight gain than wild-type animals, and improved glucose tolerance, better insulin sensitivity and markedly diminished adipose tissue inflammation. This suggests MNK2 plays a role in adipogenesis and/or lipogenesis and in macrophage biology. MNK1-KO/HFD mice show better glucose tolerance and insulin sensitivity, but gain weight and show similar adipose inflammation to WT animals. These data suggest MNK1 participates in mediating HFD-induced insulin resistance. Our findings reveal distinct roles for the MNKs in a novel area of disease biology, metabolic dysfunction, and suggests they are potential new targets for managing metabolic disease.