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

•Autophagy is up-regulated in the human adipose tissue in obesity and type 2 diabetes with the prevalence to visceral AT.•Obesity may contribute to autophagy-related increase of apoptosis in subcutaneous AT.•In visceral AT both autophagy and apoptosis were only evident in patients who developed obesity-associated T2D.•Increased autophagy in obese and T2D patients occurred together with AT inflammation.

BackgroundPathophysiology 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 findingsNumerous 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.ConclusionsOur 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.