Maldonado-Ruiz R, Montalvo-Martínez L, Fuentes-Mera L, Camacho A
Neuroscience Unit, Center for Research and Development in Health Sciences, Autonomous University of Nuevo Leon, Leon, Mexico.
Laboratory of Virology and Immunology, Faculty of Life Sciences, Autonomous University of Nuevo Leon, Leon, Mexico.
Nutr Diabetes. 2017 Mar 20;7(3):e254. doi: 10.1038/nutd.2017.10.
Obesity is an energy metabolism disorder that increases susceptibility to the development of metabolic diseases. Recently, it has been described that obese subjects have a phenotype of chronic inflammation in organs that are metabolically relevant for glucose homeostasis and energy. Altered expression of immune system molecules such as interleukins IL-1, IL-6, IL-18, tumor necrosis factor alpha (TNF-α), serum amyloid A (SAA), and plasminogen activator inhibitor-1 (PAI-1), among others, has been associated with the development of chronic inflammation in obesity. Chronic inflammation modulates the development of metabolic-related comorbidities like metabolic syndrome (insulin resistance, glucose tolerance, hypertension and hyperlipidemia). Recent evidence suggests that microglia activation in the central nervous system (CNS) is a priority in the deregulation of energy homeostasis and promotes increased glucose levels. This review will cover the most significant advances that explore the molecular signals during microglia activation and inflammatory stage in the brain in the context of obesity, and its influence on the development of metabolic syndrome and type two diabetes.
肥胖是一种能量代谢紊乱疾病，会增加患代谢性疾病的易感性。最近有研究表明，肥胖个体在与葡萄糖稳态和能量代谢相关的器官中具有慢性炎症表型。免疫系统分子如白细胞介素IL-1、IL-6、IL-18、肿瘤坏死因子α（TNF-α）、血清淀粉样蛋白A（SAA）和纤溶酶原激活物抑制剂-1（PAI-1）等的表达改变，与肥胖中慢性炎症的发展有关。慢性炎症会调节代谢相关合并症的发展，如代谢综合征（胰岛素抵抗、糖耐量异常、高血压和高脂血症）。最近的证据表明，中枢神经系统（CNS）中的小胶质细胞激活是能量稳态失调的首要因素，并会促使血糖水平升高。本综述将涵盖在肥胖背景下探索大脑中小胶质细胞激活和炎症阶段的分子信号及其对代谢综合征和2型糖尿病发展的影响的最重要进展。
