II型糖尿病常常是由进食高脂饮食引起的，它会导致肥胖症。一项新的研究显示，JNK基因在与高脂饮食生活方式有关的代谢改变及炎症中扮演着一个至关重要的角色。这些发现为JNK可能成为糖尿病治疗的一个强有力的标靶而增添了证据。许多不同类型的细胞都会表达JNK 基因，其中包括巨噬细胞。人们已知这些在脂肪组织中发现的免疫细胞会刺激导致疾病的炎症。
Sook Myoung Han及其同事在小鼠的巨噬细胞中删除了JNK1 和 JNK2基因。与对照小鼠相比，尽管没有JNK基因的小鼠当被喂食高脂饮食时其体重会有相同的增量，但它们不会出现胰岛素抵抗性和糖尿病。研究人员还看到巨噬细胞在该动物的脂肪组织中的出现减少了。
这些结果提示，当受到高脂饮食的驱动时，JNK基因可诱发导致糖尿病的炎症。（生物谷Bioon.com）
doi:10.1126/science.1227568
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JNK Expression by Macrophages Promotes Obesity-Induced Insulin Resistance and Inflammation
Myoung Sook Han, Dae Young Jung, Caroline Morel, Saquib A. Lakhani, Jason K. Kim, Richard A. Flavell, and Roger J. Davis
The cJun NH2-terminal kinase (JNK) signaling pathway contributes to inflammation and plays a key role in the metabolic response to obesity, including insulin resistance. Macrophages are implicated in this process. To test the role of JNK, we established mice with selective JNK-deficiency in macrophages. We report that feeding a high-fat diet to control and JNK-deficient mice caused similar obesity, but only mice with JNK-deficient macrophages remained insulin sensitive. The protection of mice with macrophage-specific JNK-deficiency against insulin resistance was associated with reduced tissue infiltration by macrophages. Immunophenotyping demonstrated that JNK was required for proinflammatory macrophage polarization. These studies demonstrate that JNK in macrophages is required for the establishment of obesity-induced insulin resistance and inflammation.
