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Título

Attenuated metabolism is a hallmark of obesity as revealed by comparative proteomic analysis of human omental adipose tissue

AutorPérez-Pérez, Rafael CSIC ORCID; García-Santos, Eva CSIC; Ortega, Francisco J.; López, Juan A.; Camafeita, Emilio; Ricart, Wifredo; Fernández-Real, José M.; Peral, Belén CSIC ORCID
Palabras claveObesity
TKT
ACY-1
2D-DIGE
MALDI-MS
Fecha de publicación1-oct-2011
EditorElsevier
CitaciónJournal of Proteomics 75(3): 783-795 (2012)
ResumenObesity is recognized as an epidemic health problem worldwide. In humans, the accumulation of omental rather than subcutaneous fat appears to be tightly linked to insulin resistance, type 2 diabetes and cardiovascular disease. Differences in gene expression profiles in the adipose tissue comparing non-obese and obese subjects have been well documented. However, to date, no comparative proteomic studies based on omental fat have investigated the influence of obesity in protein expression. In this work, we searched for proteins differentially expressed in the omental fat of non-obese and obese subjects using 2D-DIGE and MS. Forty-four proteins, several of which were further studied by immunoblotting and immunostaining analyses, showed significant differences in the expression levels in the two groups of subjects. Our findings reveal a clearly distinctive proteomic profile between obese and non-obese subjects which emphasizes: i) reduced metabolic activity in the obese fat, since most down-regulated proteins were engaged in metabolic pathways; and ii) morphological and structural cell changes in the obese fat, as revealed by the functions exerted by most up-regulated proteins. Interestingly, transketolase and aminoacylase-1 represent newly described molecules involved in the pathophysiology of obesity, thus opening up new possibilities in the study of obesity.
DescripciónEl pdf del artículo es el manuscrito de autor.
Versión del editorhttp://dx.doi.org/10.1016/j.jprot.2011.09.016
URIhttp://hdl.handle.net/10261/42202
DOI10.1016/j.jprot.2011.09.016
ISSN1874-3919
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