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LETTERS TO THE EDITOR |
NutriGuard Research
1051 Hermes Avenue
Encinitas, CA 92024
E-mail: mccarty{at}pantox.com
Dear Sir:
With regard to the recent report by Chiu et al (1), which shows a direct correlation between plasma 25-hydroxyvitamin D and insulin sensitivity, it is surprising that the authors do not cite their own highly germane study, which shows that insulin sensitivity correlates inversely with plasma parathyroid hormone (PTH) in healthy volunteers (2). There is reason to suspect that mild secondary hyperparathyroidism may be the chief mediator of the insulin resistance associated with poor vitamin D status (3). PTH can increase free intracellular calcium concentrations in key insulin target tissues, including adipocytes and skeletal muscle (4, 5). Reusch et al (6) have shown that moderate increases in free intracellular calcium can compromise the efficiency of insulin-stimulated glucose uptake, not by interfering with the activation of PI3K-Akt but rather by suppressing the activation of a phosphatase required for optimal function of GLUT-4. Indeed, both primary and secondary hyperparathyroidism are characterized by reduced insulin sensitivity (3). The findings of Chiu et al's group suggest that the relatively modest increases in plasma PTH associated with suboptimal vitamin D status may likewise have implications for insulin function.
If this thesis is correct, one would expect supplemental calcium to affect insulin sensitivity, at least in subjects with mildly elevated PTH. In fact, there are 2 controlled studies that showed that supplemental calcium improves insulin sensitivity in hypertensive persons (7, 8). Moreover, a relatively high calcium intake has been linked to a reduced risk of diabetes in a prospective epidemiologic study (9). Chiu et al's article cites the scarce findings relevant to the effect of supplemental vitamin D on insulin sensitivity. It would be of great interest to determine whether effective supplemental intakes of vitamin D (10)—with or without concurrent supplemental calcium—can indeed improve the insulin sensitivity of groups with mediocre vitamin D status.
Because it seems unlikely that insulin function would influence 25-hydroxyvitamin D concentrations, it is reasonable to presume that the latter is influencing the former. However, a skeptic might note that frequent outdoor exercise would tend to improve both vitamin D status and insulin sensitivity and thus might account for the correlation observed by Chiu et al. To discount this argument, it would be helpful if the authors assessed and analyzed the exercise habits of their subjects.
REFERENCES
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