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首页> 外文期刊>Cell metabolism >Jejunal T Cell Inflammation in Human Obesity Correlates with Decreased Enterocyte Insulin Signaling
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Jejunal T Cell Inflammation in Human Obesity Correlates with Decreased Enterocyte Insulin Signaling

机译：人肥胖中的空肠T细胞炎症与肠细胞胰岛素信号转导减少有关

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摘要

In obesity, insulin resistance is linked to inflammation in several tissues. Although the gut is a very large lymphoid tissue, inflammation in the absorptive small intestine, the jejunum, where insulin regulates lipid and sugar absorption is unknown. We analyzed jejunal samples of 185 obese subjects stratified in three metabolic groups: without comorbidity, suffering from obesity-related comorbidity, and diabetic, versus 33 lean controls. Obesity increased both mucosa surface due to lower cell apoptosis and innate and adaptive immune cell populations. The preferential CD8 alpha b T cell location in epithelium over lamina propria appears a hallmark of obesity. Cytokine secretion by T cells from obese, but not lean, subjects blunted insulin signaling in enterocytes relevant to apical GLUT2 mislocation. Statistical links between T cell densities and BMI, NAFLD, or lipid metabolism suggest tissue crosstalk. Obesity triggers T-cell-mediated inflammation and enterocyte insulin resistance in the jejunum with potential broader systemic implications.
机译：在肥胖症中，胰岛素抵抗与几种组织的炎症有关。尽管肠道是非常大的淋巴组织，但尚不清楚胰岛素调节脂质和糖吸收的吸收性小肠空肠的炎症。我们分析了分为三个代谢组的185名肥胖受试者的空肠样本：无合并症，患有与肥胖相关的合并症和糖尿病的人，而有33个瘦对照。肥胖由于细胞凋亡降低以及先天性和适应性免疫细胞群增加而增加了粘膜表面。固有层上皮细胞中CD8 alpha b T细胞的优先定位是肥胖的标志。肥胖但非瘦的受试者的T细胞分泌的细胞因子使与顶端GLUT2错位有关的肠上皮细胞的胰岛素信号减弱。 T细胞密度与BMI，NAFLD或脂质代谢之间的统计联系表明组织串扰。肥胖会触发空肠中T细胞介导的炎症和肠上皮胰岛素抵抗，并可能具有更广泛的全身意义。

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