Abstract
The adipokine CTRP-3 (C1q/TNF-related protein-3) exerts anti-inflammatory and anti-diabetic effects. Its regulation in obesity and during weight loss is unknown. Serum and adipose tissue (AT) samples were obtained from patients (n = 179) undergoing bariatric surgery (BS). Moreover, patients (n = 131) participating in a low-calorie diet (LCD) program were studied. CTRP 3 levels were quantified by ELISA and mRNA expression was analyzed in AT and in 3T3-L1 adipocytes treated with bile acids and incretins. There was a persistent downregulation of CTRP-3 serum levels during weight loss. CTRP-3 expression was higher in subcutaneous than in visceral AT and serum levels of CTRP-3 were positively related to AT expression levels. A rapid decrease of circulating CTRP-3 was observed immediately upon BS, suggesting weight loss-independent regulatory mechanisms. Adipocytes CTRP-3 expression was inhibited by primary bile acid species and GLP 1. Adipocyte-specific CTRP-3 deficiency increased bile acid receptor expression. Circulating CTRP-3 levels are downregulated during weight loss, with a considerable decline occurring immediately upon BS. Mechanisms dependent and independent of weight loss cause the post-surgical decline of CTRP-3. The data strongly argue for regulatory interrelations of CTRP-3 with bile acids and incretin system.
Highlights
Among the increasing number of secretory proteins that have been identified as so-called adipo(cyto)kines, the family of C1q/TNF-related proteins (CTRPs) comprises 15 distinct adiponectin paralogs [1]
Significantly downregulated CTRP-3 expression in adipocytes, whereas GIP caused a non-significant trend in lowering CTRP-3 expression. These findings suggest for the first time that the rapid decline of circulating CTRP-3 levels after bariatric surgery might be caused by specific regulatory effects of certain incretins and bile acid sub-species in adipocytes and adipose tissue
The present study reports a highly significant decrease of circulating CTRP-3 levels by either surgical or dietary intervention, indicating a general, negative regulation of systemic CTRP-3 during weight loss
Summary
Among the increasing number of secretory proteins that have been identified as so-called adipo(cyto)kines, the family of C1q/TNF-related proteins (CTRPs) comprises 15 distinct adiponectin paralogs [1]. CTRP-3 as a prominent and pleiotropic CTRP is mainly expressed in adipose tissue and in gonads and kidney [2] It represents a mainly anti-inflammatory adipokine in the context of cell proliferation [3,4,5], metabolism [6,7], and inflammation [8,9,10]. CTRP-3 regulates hepatic carbohydrate and lipid metabolism [6,11] as well as adipogenesis [8] It has immunomodulatory properties with anti-inflammatory effects locally in adipose tissue [8,9,12] and systemically [7,9]. Data on local CTRP-3 gene expression in adipose tissue compartments in obesity and on the regulation of systemic CTRP-3 during weight loss is of physiological importance
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