Previous studies have yielded conflicting findings on the relationship between low vitamin D (25-OH-D) and impaired glucose homeostasis. In this context, we hypothesized that combined assessment of 25-OH-D with its regulator parathyroid hormone (PTH) may be required for optimal evaluation of the impact of vitamin D status on glucose metabolism. Thus, we evaluated the prospective associations of 25-OH-D and PTH at 3-months postpartum with beta-cell function (Insulin Secretion-Sensitivity Index-2 (ISSI-2)), insulin sensitivity (Matsuda index) and glycemia at 12-months postpartum in 494 women undergoing serial metabolic characterization. Notably, 32% of those with pre-diabetes/diabetes at 12-months postpartum had both vitamin D deficiency and PTH in the highest tertile at 3-months postpartum. On multiple-adjusted linear regression analyses, vitamin D deficiency/insufficiency with PTH in the highest tertile at 3-months independently predicted poorer beta-cell function (P=0.03) and insulin sensitivity (P=0.01), and increased fasting (P=0.03) and 2-hour glucose (P=0.002) at 12-months postpartum. In contrast, vitamin D deficiency/insufficiency with lower PTH did not predict these outcomes. In conclusion, only vitamin D deficiency/insufficiency with increased PTH is an independent predictor of beta-cell dysfunction, insulin resistance and glycemia, highlighting the need for consideration of the PTH/25-OH-D axis when studying the impact of vitamin D status on glucose homeostasis.
- Received March 25, 2014.
- Accepted May 20, 2014.
- © 2014 by the American Diabetes Association.
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