Intracellular inflammatory pathways in visceral adipose tissue from non obese, high IR-MO and T2D-MO individuals.

<p>(<b>A</b>) Expression and phosphorylation of JNK 1/2 isoforms: All obese patients, independently of high degree of insulin resistance and diabetes state, had significantly elevated levels of JNK 1 and 2 expression and phosphorylation versus lean group. (<b>B</b>) Expression and activation of ERK1/2 isoforms: All samples had similar levels of constitutive ERK 1/2 expression. VAT of lean subjects showed an undetectable ERK1/2 activation, in contrast to the high levels of ERK 1/2 activation seen in morbid obese patients (high IR-MO and T2D-MO). No significant differences were observed between both obese groups. (<b>C</b>) Expression and phosphorylation of STAT3: Both, phosphorylation and expression of STAT3 were significantly increased in VAT from MO individuals versus lean controls. Although there were not differences in the observed phosphorylation of STAT3 between high IR-MO and diabetic groups, elevated levels of expression were seen in diabetic individuals comparing with high IR-MO. (<b>D</b>) NF-κB pathway: There was a significant increase of IκB-α mRNA expression in VAT of MO compared to non obese subjects. Moreover, there were no significant differences in the high levels observed in both morbidly obese groups. EMSA technique revealed that NF-κB activation was significantly elevated in VAT of MO patients compared to the low levels seen in lean individuals. NF-κB activity levels were similar when the MO group was divided in high IR and T2D subgroup. Significant differences (Duncan; p<0.05) are indicated with different words.