Abstract
Contribution of individual adiponectin isoforms to lipolysis regulation remains unknown. We investigated the impact of full-length, trimeric and globular adiponectin isoforms on spontaneous lipolysis in subcutaneous abdominal (SCAAT) and visceral adipose tissues (VAT) of obese and non-obese subjects. Furthermore, we explored the role of AMPK (5'-AMP-activated protein kinase) in adiponectin-dependent lipolysis regulation and expression of adiponectin receptors type 1 and 2 (AdipoR1 and AdipoR2) in SCAAT and VAT. Primary adipocytes isolated from SCAAT and VAT of obese and non-obese women were incubated with 20 µg/ml of: A) full-length adiponectin (physiological mixture of all adiponectin isoforms), B) trimeric adiponectin isoform or C) globular adiponectin isoform. Glycerol released into media was used as a marker of lipolysis. While full-length adiponectin inhibited lipolysis by 22% in non-obese SCAAT, globular isoform inhibited lipolysis by 27% in obese SCAAT. No effect of either isoform was detected in non-obese VAT, however trimeric isoform inhibited lipolysis by 21% in obese VAT (all p<0.05). Trimeric isoform induced Thr172 p-AMPK in differentiated preadipocytes from a non-obese donor, while globular isoform induced Ser79 p-ACC by 32% (p<0.05) and Ser565 p-HSL by 52% (p = 0.08) in differentiated preadipocytes from an obese donor. AdipoR2 expression was 17% and 37% higher than AdipoR1 in SCAAT of obese and non-obese groups and by 23% higher in VAT of obese subjects (all p<0.05). In conclusion, the anti-lipolytic effect of adiponectin isoforms is modified with obesity: while full-length adiponectin exerts anti-lipolytic action in non-obese SCAAT, globular and trimeric isoforms show anti-lipolytic activity in obese SCAAT and VAT, respectively.
Highlights
Excessive accumulation of adipose tissue is associated with development of multiple metabolic and cardiovascular abnormalities including insulin resistance and type 2 diabetes [1,2]
Spontaneous lipolysis in SCAAT but not visceral adipose tissue (VAT) was positively associated with BMI (r = 0.56, p,0.05) in obese, while no association was observed in non-obese subjects in either localization
The major finding is that lipolysis is inhibited by globular adiponectin in SCAAT and by trimeric isoform in VAT, while no effect of full-length adiponectin was observed in either depot of obese subjects, while full-length adiponectin was effective in SCAAT of non-obese subjects
Summary
Excessive accumulation of adipose tissue is associated with development of multiple metabolic and cardiovascular abnormalities including insulin resistance and type 2 diabetes [1,2]. Higher plasma FFA levels were repeatedly observed in obese and insulin-resistant subjects compared to lean individuals, probably due to increased delivery of FFA from enlarged adipose tissue [5,6,7]. Several impairments in the control of lipolysis were documented in obese subjects including altered sensitivity to major regulators of lipolysis such as catecholamines, insulin and natriuretic peptides [4,8]. Our group has shown that adiponectin - a cytokine with marked anti-inflammatory, anti-atherogenic and insulin-sensitizing properties [13], inhibits spontaneous as well as catecholamineinduced lipolysis in non-obese subjects, while this effect was lost in obesity [14]
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