Proinflammatory Circulating Factors in Non-alcoholic Fatty Liver Disease Associated to Metabolic Syndrome.

LUCERO, DIEGO; ZAGO, VALERIA; LÓPEZ, GRACIELA; MIKSZTOWICZ, VERÓNICA; FAINBOIM, HUGO3; GRAFFIGNA, MABEL; WIKINSKI, REGINA1; BRITES, FERNANDO; BERG GABRIELA; SCHREIER, LAURA

Hamburgo. Alemania

Congreso; 78th European Atherosclerosis Society Congress; 2010

European Atherosclerosis Society

Non-alcoholic fatty liver (NAFL) is another component of the metabolic syndrome (MS) that it might be associated with alterations in circulating proinflammatory factors which would contribute to cardiovascular disease risk. Our aim was to measure plasma inflammatory markers in NAFL associated to MS. We studied 68 patients with MS (ATP III). Abdominal ultrasonographies were performed by a single operator, and patients were divided into two groups according to the presence (group A) or the absence (group B) of NAFL. Blood was drawn after 12 hour fasting. Lipid profile and the levels of free fatty acids (FFA), adiponectin, TNF-á, CRPhs, VCAM-1 and ICAM-1 were measured in serum. Triglycerides and FFA were higher in group A (p<0.05). There were no differences in TNF-á, VCAM-1 and ICAM-1 between groups. Adiponectin presented a significant reduction in group A (media±SD: 6.7±2.4 vs. 9.0±6.2 µg/ml; p=0.04) independently of HOMA-IR, while CRPhs was higher (median, range: 2.2, 0.3-9.3 vs. 1.2, 0.1-3.7 mg/l, p<0.02) and correlated with all the inflammatory markers: TNF-á (r=0.34, p<0.02), VCAM-1 (r=0.29; p<0.03), ICAM-1 (r=0.56; p<0.01), adiponectin (r=-0.34; p=0.04) and FFA (r=0.35; p<0.05). Also, opposite correlations were observed with FFA and TNF-á (r=0.36; p<0.04) and with FFA and adiponectin (r=-0.40; p<0.03) even after adjusting by insulin-resistance factors. The increase in FFA influx from adipose tissue to the liver is closely linked to an inflammatory state. NAFL would constitute a low chronic inflammatory condition, represented in plasma by higher CRPhs levels and lower adiponectin concentration, independent of the presence of insulin resistance.