ICEECE2012 Poster Presentations Obesity (114 abstracts)
1CIBERDEM, Hospital Universitari Joan XXIII, Pere Virgili Institute, Tarragona, Spain; 2Servicio de Endocrinología y Nutrición, Hospital Clínico Virgen de la Victoria, Málaga, Spain; 3Ciber Fisiopatología Obesidad y Nutrición (CIBEROBN), Málaga, Spain; 4Fundación IMABIS, Málaga, Spain.
Objective: Zinc-α2 glycoprotein (ZAG) stimulates lipid loss by adipocytes and may be involved in the regulation of adipose tissue metabolism. We analyze ZAG expression levels in adipose tissue from a group of morbidly obese patients, and their relationship with lipogenic and lipolytic genes and with insulin resistance (IR).
Design: mRNA expression levels of PPARgamma, IRS-1, IRS-2, lipogenic and lipolytic genes and ZAG were quantified in visceral (VAT) and subcutaneous adipose tissue (SAT) of 25 nondiabetic morbidly obese patients, 11 with low IR and 14 with high IR. Plasma ZAG was determined by ELISA.
Results: The morbidly obese patients with low IR had a significantly higher ZAG gene expression in VAT as compared with the patients with high IR (P=0.023). In the patients with low IR, the VAT ZAG gene expression was significantly greater than that in SAT (P=0.009). ZAG expression correlated strongly between SAT and VAT (r=0.709, P<0.001). In VAT, ZAG expression correlated significantly and positively with the expression of PPARgamma, ACSS2, DGAT1, ATGL, IRS-1, IRS-2 and adiponectin. In SAT, ZAG expression correlated significantly and positively with PPARgamma, ACC1, DGAT1, ATGL, HSL and adiponectin. VAT ZAG expression was mainly predicted by insulin, HOMA-IR, circulating adiponectin levels and expression of adiponectin and ACSS2. SAT ZAG expression was only predicted by expression of ATGL.
Conclusions: ZAG is involved in modulating lipid metabolism in adipose tissue and is associated with insulin resistance.
Declaration of interest: I declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This work was supported. Instituto de Salud Carlos III (PS09/01060, PS09/00997).