期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 409, 期 C, 页码 21-32出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2015.03.015
关键词
Obesity; T2D; Autophagy; Adipose tissue; Inflammation
资金
- Deutsche Diabetes Gesellschaft [934000-917]
- Kompetenznetz Adipositas (Competence Network for Obesity) - Federal Ministry of Education and Research (German Obesity Biomaterial Bank)
- Deutsche Forschungsgemeinschaft [SFB 1052/1, B01]
- Helmholtz Alliance ICEMED - Imaging and Curing Environmental Metabolic Diseases, through the Initiative and Networking Fund of the Helmholtz Association [934000-972]
- [FKZ 01GI1128]
- [FKZ: 01EO1001]
- [K7-64]
Background: Pathophysiology of obesity is closely associated with enhanced autophagy in adipose tissue (AT). Autophagic process can promote survival or activate cell death. Therefore, we examine the occurrence of autophagy in AT of type 2 diabetes (T2D) patients in comparison to obese and lean individuals without diabetes. Methodology/principal findings: Numerous autophagosomes accumulated within adipocytes were visualized by electron transmission microscopy and by immunofluorescence staining for autophagy marker LC3 in obese and T2D patients. Increased autophagy was demonstrated by higher LC3-II/LC3-I ratio, upregulated expression of LC3 and Atg5 mRNA, along with decreased p62 and mTOR protein levels. Increased autophagy occurred together with AT inflammation. Conclusions: Our data suggest fat depot-related differences in autophagy regulation. In subcutaneous AT, increased autophagy is accompanied by increased markers of apoptosis in patients with obesity independently of T2D. In contrast, in visceral AT only in T2D patients increased autophagy was related to higher markers of apoptosis. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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