Obesity modifies expression profiles of metabolic markers in superficial and deep subcutaneous abdominal adipose tissue depots.

While visceral adipose tissue (VAT) associates to obesity, there is debate for subcutaneous adipose tissue (SAT). One explanation may be SAT subcompartments, superficial-SAT (sSAT) and deep-SAT (dSAT), recently recognized as independent depots. Our aim was to establish roles for sSAT/dSAT with obesity by examining the expression of proteins key to adipocyte metabolism. Paired biopsies from sSAT and dSAT of 10 normal-weight (BMI 21.8 ± 0.8 kg/m(2)) and 11 obese subjects (BMI 44 ± 2.1 kg/m(2)) were analyzed for differences in insulin sensitivity using adiponectin, GLUT4 and resistin, glucocorticoid metabolism by 11βHSD1 and alterations of the adipokines leptin and TNFα. Between lean and obese subjects, sSAT and dSAT changes for GLUT4, resistin and TNFα were equivalent. Resistin and TNFα increased in both obese SAT sub-compartments; 33-fold (sSAT; P < 0.006) and 18.5-fold (dSAT; P < 0.003) higher resistin, with undetectable in leans to significant TNFα levels in obese. In contrast, GLUT4 showed 5.5-fold (sSAT; P < 0.03) and 7-fold (dSAT; P < 0.03) lower levels in obese, correlating to BMI (r = -0.6423, P = 0.007) and HOMA-IR (r = -0.5882, P = 0.017). Exclusive sSAT-specific differences were observed for adiponectin, leptin, and 11βHSD1. Both sSAT 11βHSD1 and leptin increased in obese, with 11βHSD1 2.5-fold (P = 0.052) and leptin 3.3-fold (P < 0.008) higher, with 11βHSD1 correlating to HOMA-IR (r = 0.5203, P = 0.0323) and leptin to BMI (r = 0.5810, P = 0.01). In contrast, obese had 7-fold (P < 0.02) lower sSAT adiponectin, correlating to BMI (r = -0.5178, P = 0.027) and HOMA-IR (r = -0.4570, P = 0.049). Overall, sSAT and dSAT are distinct abdominal adipose tissue depots with independent metabolic functions. Between the two, sSAT shows clear independent effects that associate to obesity and its metabolic complications.