We thank Hjelmesæth et al. (1) for their comments on our recent publication (2). It would be ideal to evaluate the effects of plasma parathyroid hormone (PTH), calcium, and 25-hydroxyvitamin D [25(OH)D] simultaneously on metabolic syndrome; however, with limited plasma samples, neither PTH nor calcium could be measured in our study. Nonetheless, besides reporting that PTH level was associated with metabolic syndrome only in older men but not in older women or young participants, Reis et al. (3) also reported that the association between 25(OH)D level and metabolic syndrome was independent to PTH levels and calcium intake. It is true that PTH but not 25(OH)D was associated with metabolic syndrome in the Rancho Bernardo cohort (4), but the mean 25(OH)D concentration in this population was remarkably higher (108.9 nmol/l) than that in other study populations in which vitamin D deficiency commonly occurred among participants. Moreover, although controlling for PTH, calcium, and IGF-1 only yielded a marginal association between 25(OH)D and the metabolic syndrome risk z score in the Medical Research Council Ely Prospective Study (5), the significant associations between higher baseline 25(OH)D and lower future fasting insulin and insulin resistance levels were found to be independent of PTH and calcium. In addition, previous studies from in vitro and in vivo suggested that vitamin D could modulate insulin receptor gene, insulin gene and PPARD gene expression, and/or calcium flux (6). Taken together, the existing evidence has demonstrated that vitamin D may have an important role in the development of metabolic diseases, along with the effects of PTH and many other factors. Given the complicated relationships among vitamin D, PTH, and calcium, large-scale and well-designed clinical trials are needed to confirm the specific roles of vitamin D, PTH, and calcium in the pathogenesis of metabolic disorders.
Acknowledgments
No potential conflicts of interest relevant to this article were reported.
