Resistin induces lipolysis and suppresses adiponectin secretion in cultured human visceral adipose tissue

Abstract

Resistin is an adipokine secreted from adipose tissue, which is likely involved in the development of obesity and insulin resistance via its interaction with other organs, as well as affecting adipose tissue function. The impact of resistin treatment on lipolysis and adiponectin secretion in human visceral adipose tissue is currently unknown. Mesenteric adipose tissue samples were obtained from 14 male subjects [age 54 ± 6 yr, body mass index (BMI) 23.59 ± 0.44 kg/m²] undergoing abdominal surgeries. Adipose tissues were cultured and treated with resistin (100 ng/mL, 24 h) in the absence or presence of different signaling inhibitors: H89 (1 μM), PD98059 (25 μM) and SB201290 (20 μM) for glycerol and non-esterified fatty acid (NEFA) measurement. Adiponectin level from media at 24 h was also measured via ELISA. Adipose tissue minces after resistin incubation (100 ng/mL, 24 h) were also collected for further Western blotting analysis.

Resistin resulted in significant induction of glycerol (3.62 ± 0.57 vs. 5.30 ± 1.11 mmol/L/g tissue, p < 0.05) and NEFA (5.99 ± 1.06 vs. 8.48 ± 1.57 mmol/L/g tissue, p < 0.05) release at 24 h. H89 and PD98059 partially inhibited resistin induced glycerol and NEFA release, while SB201290 has no such effect. Resistin induced the phosphorylation of p-HSL at serine 563, PKA at ~ 62 kDa and ERK1/2 as measured by Western blotting. Resistin led to significant reduction of the secretion of adiponectin (38.16 ± 10.43 vs. 21.81 ± 4.21 ng/mL/g tissue, p < 0.05). Our current findings implicate that resistin might play a significant role in obesity related pathologies in various tissues via its effect on adipose tissue function.