The
orphan nuclear receptors (ONRs),
retinoic acid receptor-related orphan receptor γ-1 (RORγ1) and
peroxisome proliferator-activated receptor γ-2 (PPARγ2), are central mediators controlling adipocyte (AD) differentiation. Through their distinct tissue distribution and specific target gene activation, ONRs control diverse aspects of
fatty acid metabolism and
insulin sensitivity. Adding further complexity,
obesity begets resistance to
insulin signals and can ultimately result in diabetes. In this study, we investigate whether there are differences in the RORγ1 and PPARγ2 expression in visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) from
morbid obesity (MO) individuals either
insulin resistant (high-IR MO) or
insulin sensitivity (low-IR MO). Our results indicate for the first time in human the RORγ1
mRNA and
protein expression levels and activation with coactivator, such as
peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α) were higher in the VAT from high-IR MO. In contrast, PPARγ2 expression and activation were higher in the VAT from low-IR MO. In this way, we have also found a positive association between RORγ1
mRNA and
protein expression with many components of
metabolic syndrome, with a strong dependence of
insulin and HOMA(IR) index in VAT, but not in SAT. Our data suggest that RORγ1 may be added to the growing list of
nuclear receptors in adipose tissue use to modulate the
insulin resistance associated to the
obesity. Measurement of RORγ1 and PPARγ2 in adipose tissue might be useful for evaluating the outcomes of various clinical interventions for
obesity-related diabetes type II.