We thank Tsuzaki et al. (1) for their comments and for the interesting data they share. The association of serum adiponectin concentration with LDL particle size in middle-aged and elderly Japanese adults confirms our findings in young Israeli adults, points to the generalizability of the findings, and demonstrates that the association is independent of several single nucleotide polymorphisms affecting adiponectin levels.

Higher adiponectin levels are associated with a favorable pattern of lipid depot partitioning characterized by a lower proportion of subcutaneous fat relative to intra-abdominal fat and greater insulin sensitivity (2). Additionally, changes in adiponectin correlate well with alterations in lipid metabolism in response to therapeutic interventions (3). Adiponectin rises in response to agents such as pioglitazone, which affects lipid partitioning, improves the lipid profile, and increases LDL particle size (4). Of note, as adiponectin concentration tends to vary among individuals of different ethnic backgrounds (5), it may be useful to determine its relation with the relative portion of small LDL to total LDL cholesterol in ethnically diverse populations to draw inferences as to the potential clinical impact or assess the metabolic response to therapeutic interventions (6). Future research is needed to determine the precise mechanistic link and specific metabolic pathways by which adiponectin (both high and low molecular weight moieties) affects lipoprotein metabolism.

No potential conflicts of interest relevant to this article were reported.

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