دورية أكاديمية

Intervertebral disc degeneration in mice with type II diabetes induced by leptin receptor deficiency

التفاصيل البيبلوغرافية
العنوان: Intervertebral disc degeneration in mice with type II diabetes induced by leptin receptor deficiency
المؤلفون: Xinhua Li, Xiaoming Liu, Yiru Wang, Fuming Cao, Zhaoxiong Chen, Zhouyang Hu, Bin Yu, Hang Feng, Zhaoyu Ba, Tao Liu, Haoxi Li, Bei Jiang, Yufeng Huang, Lijun Li, Desheng Wu
المصدر: BMC Musculoskeletal Disorders, Vol 21, Iss 1, Pp 1-10 (2020)
بيانات النشر: BMC, 2020.
سنة النشر: 2020
المجموعة: LCC:Diseases of the musculoskeletal system
مصطلحات موضوعية: Diabetes, Leptin receptor, Intervertebral disc degeneration, Diseases of the musculoskeletal system, RC925-935
الوصف: Abstract 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
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1471-2474
Relation: https://doaj.org/toc/1471-2474
DOI: 10.1186/s12891-020-3091-1
URL الوصول: https://doaj.org/article/eb255eaf6f994369aa6b4826b6d35e6b
رقم الأكسشن: edsdoj.b255eaf6f994369aa6b4826b6d35e6b
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14712474
DOI:10.1186/s12891-020-3091-1