肥胖和2型糖尿病对椎间盘退变影响的研究进展  

Research progress in influence of obesity and type 2 diabetes mellitus on intervertebral disc degeneration

作　　者：秦志琳[1] 江华[2] QIN Zhilin;JIANG Hua(Health Management Center,Jiangbin Hospital of Guangxi Zhuang Autonomous Region,Nanning 530021,China;Department of Spine Surgery,the First Affiliated Hospital of Guangxi Medical University,Nanning 530021,China)

机构地区：[1]广西壮族自治区江滨医院健康管理中心,南宁530021 [2]广西医科大学第一附属医院脊柱骨病外科,南宁530021

出　　处：《广西医科大学学报》2024年第12期1677-1684,共8页Journal of Guangxi Medical University

基　　金：国家自然科学基金资助项目(No.82360438);广西自然科学基金区域高发疾病研究联合专项资助(No.2024GXNSFDA010043)。

摘　　要：肥胖(OB)和2型糖尿病(T2DM)是两种常见的代谢性疾病,与椎间盘退变(IDD)密切相关。OB可能通过增加脊柱的机械应力以及促进白色脂肪组织分泌脂肪因子而导致IDD的发生。T2DM通过影响椎间盘的血液供应和营养,并通过晚期糖基化终末产物(AGEs)诱发炎症反应,加速IDD的病理过程。脂肪细胞分泌多种脂肪因子(IL-6、TNF-α、瘦素、抵抗素和脂联素),可能参与IDD的病理生理过程。AGEs通过激活RAGE受体和NLRP3炎症小体,导致椎间盘细胞凋亡。因此,进一步阐明OB和T2DM在IDD发生和发展中的作用及其机制,将为IDD的诊治及预防提供更多策略。Obesity(OB)and type 2 diabetes mellitus(T2DM)are two common metabolic diseases that are closely related to intervertebral disc degeneration(IDD).OB may lead to the occurrence of IDD by increasing the spinal mechanical stress and promoting the secretion of adipokines by white adipose tissue.T2DM accelerates the pathological process of IDD by affecting the blood supply and nutrition of the intervertebral disc and evoking in‐flammatory reactions through advanced glycation end products(AGEs).Various adipokines,such as IL-6,TNF-α,leptin,resistin,and adiponectin,are secreted by adipocytes and may participate in the pathophysiology of IDD.In addition,AGEs cause intervertebral disc cell apoptosis by activating RAGE receptors and NLRP3 inflammasome.Therefore,further elucidating the effects and mechanisms of OB and T2DM in the initiation and progression of IDD will provide more strategies for the prevention and treatment of IDD.

关 键 词：肥胖 2型糖尿病 代谢性疾病 脂肪因子 椎间盘退变 

分 类 号：R587.2[医药卫生—内分泌] R692.9[医药卫生—内科学]