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Mol Cell Endocrinol. 2015 Jul 5;409:21-32. doi: 10.1016/j.mce.2015.03.015. Epub 2015 Mar 26.

Autophagy in adipose tissue of patients with obesity and type 2 diabetes.

Author information

1
Department of Medicine, University of Leipzig, Liebigstraße 21, D-04103 Leipzig, Germany. Electronic address: Joanna.Kosacka@medizin.uni-leipzig.de.
2
Department of Medicine, University of Leipzig, Liebigstraße 21, D-04103 Leipzig, Germany.
3
Department of Medicine, University of Leipzig, Liebigstraße 21, D-04103 Leipzig, Germany; Integrated Research and Treatment Center (IFB) Adiposity Diseases, Liebigstraße 21, D-04103 Leipzig, Germany.
4
Department of Clinical Biochemistry and Pharmacology, National Institute of Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva 84103, Israel.
5
Institute of Anatomy, University of Leipzig, Liebigstraße 13, D-04103 Leipzig, Germany.

Abstract

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, up-regulated 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.

KEYWORDS:

Adipose tissue; Autophagy; Inflammation; Obesity; T2D

PMID:
25818883
DOI:
10.1016/j.mce.2015.03.015
[Indexed for MEDLINE]

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