II型糖尿病常常是由進食高脂飲食引起的,，它會導(dǎo)致肥胖癥,。一項新的研究顯示,，JNK基因在與高脂飲食生活方式有關(guān)的代謝改變及炎癥中扮演著一個至關(guān)重要的角色,。這些發(fā)現(xiàn)為JNK可能成為糖尿病治療的一個強有力的標靶而增添了證據(jù)。許多不同類型的細胞都會表達JNK 基因,，其中包括巨噬細胞,。人們已知這些在脂肪組織中發(fā)現(xiàn)的免疫細胞會刺激導(dǎo)致疾病的炎癥。
Sook Myoung Han及其同事在小鼠的巨噬細胞中刪除了JNK1 和 JNK2基因,。與對照小鼠相比,，盡管沒有JNK基因的小鼠當被喂食高脂飲食時其體重會有相同的增量，但它們不會出現(xiàn)胰島素抵抗性和糖尿病,。研究人員還看到巨噬細胞在該動物的脂肪組織中的出現(xiàn)減少了。
這些結(jié)果提示,，當受到高脂飲食的驅(qū)動時,，JNK基因可誘發(fā)導(dǎo)致糖尿病的炎癥。（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.
