Antonio Membrives

TL;DR: The concentration of glucose, insulin, IL-6 and IGF-1 in blood are useful markers for the selection of patients with liver steatosis or NASH in morbidly obese patients.

TL;DR: Pteomic analysis of paired samples of adipocytes from subcutaneous and omental human AT revealed that both types of cells are altered in the MUHO state, and the glutathione redox cycle and other antioxidant defense systems as well as the protein-folding machinery were dysregulated and endoplasmic reticulum stress was increased in adipocyte from IR subjects.

TL;DR: The results suggest that dysregulation of both adipose tissue extracellular matrix (ECM) organization and intracellular trafficking processes may be associated with IR in obesity, and indicate that lumican and GDI2 might play depot‐dependent, pathogenic roles in obesity‐associated IR.

TL;DR: In this paper, the pathogenic processes underlying impaired adipocyte differentiation in obese individuals with insulin resistance (IR)/type 2 diabetes (T2D) were identified, and a down-regulation of a key member of the major spliceosome, PRFP8/PRP8, as observed in IR/type 2D preadipocytes from subcutaneous (SC) fat, prevented adipogenesis by altering both the expression and splicing patterns of adipogenic transcription factors and lipid droplet-related proteins.

TL;DR: In this paper, the authors demonstrate that impaired alternative splicing and dysregulated endoplasmic reticulum (ER)-associated protein degradation (ERAD) represent marker pathways of dysfunctional preadipocytes in obese individuals with insulin resistance (IR)/type 2 diabetes (T2D).