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Obes Surg. 2009 Nov;19(11):1557-63. doi: 10.1007/s11695-009-9917-4. Epub 2009 Jul 25.

YKL-40 is elevated in morbidly obese patients and declines after weight loss.

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Department of Medicine II, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.



Patients suffering from morbid obesity (MO) have an increased cardiovascular morbidity and mortality. This increased cardiovascular burden is believed to be caused by a sub-inflammatory state through an increased secretion of monocyte chemoattractant protein-1 (MCP-1) by the adipose tissue, resulting in insulin resistance (IR) and type 2 diabetes mellitus (T2DM). YKL-40, which is elevated in inflammatory processes in T2DM and IR and in ruptured plaques, might as well be involved in the increased cardiovascular burden of MO patients. The present study aims to study the level of YKL-40 in MO patients before and after weight loss as well as to investigate the relationship between YKL-40, IR, MCP-1, and obesity.


We investigated YKL-40 levels in serum samples of both 17 morbidly obese patients before and after bariatric surgery and 17 healthy controls. YKL-40 levels were determined in serum samples by enzyme-linked immunosorbent assay.


After a mean follow-up of 17.4 months and a mean weight loss of 40 kg through bariatric surgery, YKL-40 levels declined by 30.5% (p = 0.027). Multiple linear regression analysis revealed that only preoperative MCP-1 values remained independently and significantly (p = 0.001) associated with preoperative YKL-40 levels. Moreover, delta (change) homeostasis model assessment of insulin resistance (HOMA-IR) values remained independently and significantly (p = 0.002) associated with delta YKL-40 levels.


We show for the first time that elevated levels of YKL-40 in MO patients decreased after massive weight loss via bariatric surgery. YKL-40 was correlated with HOMA-IR and fasting insulin levels, indicating a role in developing processes of IR and T2DM. The tight association of MCP-1 (plaque development) and YKL-40 (plaque rupture) points to a central role of both proteins, contributing to the increased cardiovascular mortality in MO patients.

[Indexed for MEDLINE]

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