CAJ | 학술논문

肥胖和胰岛素抵抗呈现一种慢性炎性反应状态,表现为白细胞介素-6、白细胞介素-1β、巨噬细胞趋化因子等炎性反应因子水平升高.其原因在于能量代谢不平衡导致脂肪细胞肥大、增生、内质网应激和线粒体功能障碍,c-Jun氨基末端激酶(JNK)/激活蛋白(AP)-1和核因子(NF)-KB抑制蛋白激酶(IKK)β/NF-κKB两条信号通路活化,脂肪因子、游离脂肪酸和其他炎性反应介质表达增高,进而影响了全身各器官如肝脏、胰岛β细胞和骨骼肌.单核细胞和巨噬细胞是炎性反应因子另一个重要的来源.肥胖导致的JNK活化通过胰岛素受体底物-1的丝氨酸磷酸化影响胰岛素信号转导.饮食、运动、降低体重和药物可以改变炎性反应因子的水平.炎性反应理论为代谢性疾病的临床干预提供了重要的方向.
비반화이도소저항정현일충만성염성반응상태,표현위백세포개소-6、백세포개소-1β、거서세포추화인자등염성반응인자수평승고.기원인재우능량대사불평형도치지방세포비대、증생、내질망응격화선립체공능장애,c-Jun안기말단격매(JNK)/격활단백(AP)-1화핵인자(NF)-KB억제단백격매(IKK)β/NF-κKB량조신호통로활화,지방인자、유리지방산화기타염성반응개질표체증고,진이영향료전신각기관여간장、이도β세포화골격기.단핵세포화거서세포시염성반응인자령일개중요적래원.비반도치적JNK활화통과이도소수체저물-1적사안산린산화영향이도소신호전도.음식、운동、강저체중화약물가이개변염성반응인자적수평.염성반응이론위대사성질병적림상간예제공료중요적방향.
Obesity and insulin resistance are characterized by increased expression of markers and mediators of inflammation,which includes interleukin-6(IL-6),interleukin-1β(IL-1β),macrophage chemoattractant protein-1(MCP-1),etc.Chmnic energy imbalance causes adipocyte hypertrophy and hyperplasia,endoplasmic reticulum stress,and mitochondrial dysfunction.These stress induced JNK/AP-1 and IKKB/NF-κB activation which lead to increased intracellular and systemic release of adipokines,free fatty acids,and inflammatory mediators that cause adipocyte dysfunction and induce adverse effects in the liver.pancreatic B-cells and skeletal muscle.Immune cells such as mnnocytes and macrophages are another source of inflammatory factors.Obesity-induced JNK activation promotes the phosphorylation of IRS-1 at serine sites.Diet,exercise,smoking and certain drugs are also associated with different levels of inflammatory markers.The evolving concept of inflammation provides Hew opportunities for using anti-inflammatory strategies to correct the metaholic disorders.