Kou Yan-Bo, Yan Xiao-Qing, Jing Qi-Yue, Zhang Sheng-Han, Liu Zhuan-Zhuan, Wei Yan-Xia, Wang Yu-Gang
Jiangsu Key Laboratory of Immunity and Metabolism, Laboratory of Infection and Immunity, Department of Pathogenic Biology and Immunology, Xuzhou Medical University, Xuzhou, China.
Laboratory of Emergency Medicine, Second Clinical Medical College, Xuzhou Medical University, Xuzhou, China.
Biochem Biophys Res Commun. 2021 Oct 28;583:106-113. doi: 10.1016/j.bbrc.2021.10.061.
Glucose homeostasis of adipocytes could be regulated by immune-adipose crosstalk. In order to investigate the effects of Lymphotoxin-like inducible protein that competes with glycoprotein D for herpesvirus entry on T cells (LIGHT) on glucose metabolism, we performed the present study. Our results showed that LIGHT deficiency improved glucose tolerance and enhanced glucose consumption of inguinal white adipose tissue (iWAT) under high fat diet. Consistently, Light overexpression could inhibit glucose uptake during the process of white adipogenesis. Mechanistically, LIGHT interacted with lymphotoxin-β receptor (LTβR) to attenuate AKT pathway leading to downregulation of glucose transporter-4 (GLUT4) expression, which resulted in glucose uptake inhibition. In summary, our findings revealed LIGHT-LTβR-AKT-GLUT4 axis as a regulator of glucose uptake in adipose tissue, which suggested the pivotal role of LIGHT in maintaining glucose homeostasis.
脂肪细胞的葡萄糖稳态可通过免疫-脂肪相互作用来调节。为了研究与疱疹病毒进入T细胞的糖蛋白D竞争的淋巴毒素样诱导蛋白（LIGHT）对葡萄糖代谢的影响，我们开展了本研究。我们的结果表明，在高脂饮食条件下，LIGHT缺陷改善了葡萄糖耐量，并增强了腹股沟白色脂肪组织（iWAT）的葡萄糖消耗。同样，Light过表达可在白色脂肪生成过程中抑制葡萄糖摄取。从机制上讲，LIGHT与淋巴毒素-β受体（LTβR）相互作用，减弱AKT信号通路，导致葡萄糖转运蛋白4（GLUT4）表达下调，从而抑制葡萄糖摄取。总之，我们的研究结果揭示了LIGHT-LTβR-AKT-GLUT4轴是脂肪组织中葡萄糖摄取的调节因子，这表明LIGHT在维持葡萄糖稳态中起关键作用。
