机构：[1]Department of Spinal Surgery, Shanghai East Hospital, Tongji UniversitySchool of Medicine, 150 Jimo Road, Shanghai 200120, China[2]Department ofOrthopedics, Tongren Hospital, Shanghai Jiao Tong University School ofMedicine, 1111 XianXia Road, Shanghai 200336, China[3]Department ofendocrinology, Shanghai East Hospital, Tongji University School of Medicine,Shanghai 200120, China
Background The leptin receptor-deficient knockout (db/db) mouse is a well-established model for studying type II diabetes mellitus (T2DM). T2DM is an important risk factor of intervertebral disc degeneration (IVDD). Although the relationship between type I diabetes and IVDD has been reported by many studies, few studies have reported the effects of T2DM on IVDD in db/db mice model. Methods Mice were separated into 3 groups: wild-type (WT), db/db, and IGF-1 groups (leptin receptor-deficient mice were treated with insulin-like growth factor-1 (IGF-1). To observe the effects of T2DM and glucose-lowering treatment on IVDD, IGF-1 injection was used. The IVD phenotype was detected by H&E and safranin O fast green staining among db/db, WT and IGF-1 mice. The levels of blood glucose and weight in mice were also recorded. The changes in the mass of the trabecular bone in the fifth lumbar vertebra were documented by micro-computed tomography (micro-CT). Tunnel assays were used to detect cell apoptosis in each group. Results The weight of the mice were 27.68 +/- 1.6 g in WT group, which was less than 57.56 +/- 4.8 g in db/db group, and 52.17 +/- 3.7 g in IGF-1 injected group (P < 0.05). The blood glucose levels were also significantly higher in the db/db mice group. T2DM caused by leptin receptor knockout showed an association with significantly decreased vertebral bone mass and increased IVDD when compared to WT mice. The db/db mice induced by leptin deletion showed a higher percentage of MMP3 expression as well as cell apoptosis in IVDD mice than WT mice (P < 0.05), while IGF-1 treatment reversed this situation (P < 0.05). Conclusions T2DM induced by leptin receptor knockout led to IVDD by increasing the levels of MMP3 and promoting cell apoptosis. IGF-1 treatment partially rescue the phenotype of IVDD induced by leptin receptor knockout.
基金：
Key Disipline Construction Project
of Pudong Health Bureau of Shanghai (PWZxk2017–08), National Natural
Science Foundation of China (81672199), National Natural Science
Foundation of China (81371994); National Science Foundation of Jiangxi
Province, China (20171BAB205034), National Health and Family Planning
Commission Foundation of Shanghai, China (201640063); National Natural
Science Foundation of China (81572181).
第一作者机构：[1]Department of Spinal Surgery, Shanghai East Hospital, Tongji UniversitySchool of Medicine, 150 Jimo Road, Shanghai 200120, China
共同第一作者：
通讯作者：
推荐引用方式(GB/T 7714)：
Li Xinhua,Liu Xiaoming,Wang Yiru,et al.Intervertebral disc degeneration in mice with type II diabetes induced by leptin receptor deficiency[J].BMC MUSCULOSKELETAL DISORDERS.2020,21(1):doi:10.1186/s12891-020-3091-1.
APA：
Li, Xinhua,Liu, Xiaoming,Wang, Yiru,Cao, Fuming,Chen, Zhaoxiong...&Wu, Desheng.(2020).Intervertebral disc degeneration in mice with type II diabetes induced by leptin receptor deficiency.BMC MUSCULOSKELETAL DISORDERS,21,(1)
MLA：
Li, Xinhua,et al."Intervertebral disc degeneration in mice with type II diabetes induced by leptin receptor deficiency".BMC MUSCULOSKELETAL DISORDERS 21..1(2020)
