Increased circulating and visceral adipose tissue expression levels of YKL-40 in obesity-associated type 2 diabetes are related to inflammation: impact of conventional weight loss and gastric bypass
Catalán V, Gómez-Ambrosi J, Rodríguez A, Ramírez B, Rotellar F, Valentí V, Silva C, Gil MJ, Salvador J, Frühbeck G.
Plasma YKL-40 is elevated in patients with type 2 diabetes. The potential role of visceral adipose tissue (VAT) as a significant source of YKL-40 is unknown.
In the study circulating and expression levels of YKL-40 were examined in VAT analyzing the contribution of adipocytes and stromovascular fraction cells (SVFCs). We also explored YKL-40's implication in insulin resistance and inflammation and the effect of weight loss on plasma YKL-40 concentrations.
PATIENTS AND METHODS
Samples obtained from 53 subjects were used in the study. Gene and protein expression levels of YKL-40 were analyzed in VAT as well as in both adipocytes and SVFCs. In addition, circulating YKL-40 concentrations were measured before and after weight loss achieved either by Roux-en-Y gastric bypass (n = 26) or after a conventional dietetic program (n = 20).
Circulating concentrations and VAT expression of YKL-40 were increased in obese patients with type 2 diabetes (P < 0.01) as well as associated with variables of insulin resistance and inflammation. No differences in YKL-40 expression levels between adipocytes and SVFCs were detected. Monocyte chemoattractant protein-1 and homeostasis model assessment emerged (P < 0.01) as independent factors predicting circulating YKL-40. Elevated levels of YKL-40 in obese patients decreased after weight loss following a conventional hypocaloric diet (P < 0.05) but not via a surgery-induced negative energy balance mediated by the Roux-en-Y gastric bypass.
The association of increased YKL-40 mRNA and protein levels in VAT with its circulating concentrations indicates an important contribution of VAT in YKL-40 regulation. Furthermore, our data suggest a relevant role of glucose metabolism and inflammation on YKL-40 regulation.
CITATION J Clin Endocrinol Metab. 2011 Jan;96(1):200-9