We have no obvious interpretation of these associations, but previous studies have suggested that the visceral adipose tissue could be an important source of released YKL-40 in obesity [31], and since YKL-40 is known to regulate other inflammatory markers, e.g. increase the expression of monocyte chemoattractant protein-1 (MCP-1) in alveolar macrophages of patients with chronic obstructive pulmonary disease [32], it is possible that YKL-40 plays a role in orchestrating the inflammatory response originating from the visceral adipose tissue. This evidence concerns the gene CHI3L1 and obesity due to melanocortin 4 receptor deficiency.