Caroline K Kramer1, Balakumar Swaminathan, Anthony J Hanley, Philip W Connelly, Mathew Sermer, Bernard Zinman, Ravi Retnakaran. 1. Leadership Sinai Centre for Diabetes (C.K.K., B.S., A.J.H., B.Z., R.R.), Mt Sinai Hospital, Toronto, Canada M5T 3L9; Division of Endocrinology (C.K.K., A.J.H., P.W.C., B.Z., R.R.), Department of Medicine, University of Toronto, Toronto, Canada M5S 1A1; Department of Nutritional Sciences (A.J.H.), University of Toronto, Toronto, Canada M5S 1A1; Keenan Research Centre for Biomedical Science of St. Michael's Hospital (P.W.C.), Toronto, Canada M5B 1W8; Division of Obstetrics and Gynecology (M.S.), University of Toronto, Toronto, Canada M5T 3L9; and Lunenfeld-Tanenbaum Research Institute (B.Z., R.R.), Mt Sinai Hospital, Toronto, Canada M5T 3L9.
Abstract
CONTEXT: Previous studies have yielded conflicting findings on the relationship between vitamin D deficiency/insufficiency and gestational diabetes mellitus (GDM). We hypothesized that PTH may be an underlying factor relevant to this potential association. OBJECTIVE: This study sought to evaluate the effect of vitamin D and PTH status on insulin sensitivity, β-cell function, and glycemia in pregnancy. SETTING AND DESIGN: Five-hundred-twenty-four women underwent a glucose challenge test (GCT) and oral glucose tolerance test (OGTT) in late second/early third trimester. The GCT/OGTT identified 142 women with GDM, 94 with gestational impaired glucose tolerance, 163 with an abnormal GCT and normal OGTT, and 125 with normal GCT and OGTT. MAIN OUTCOMES: Glycemia was assessed by glucose tolerance status and area under the glucose curve (AUC(gluc)) on the OGTT. Insulin sensitivity and β-cell function were assessed by Matsuda index and Insulin Secretion-Sensitivity Index-2 (ISSI-2), respectively. RESULTS: There were 166 women (31.7%) with vitamin D deficiency (25-OH-D < 50 nmol/L), 178 (34%) with insufficiency (25-OH-D ≥ 50 nmol/L and < 75 nmol/L), and 180 (34.3%) with sufficiency (25-OH-D ≥ 75 nmol/L). Vitamin D status was not associated with Matsuda index, ISSI-2, AUC(gluc), or glucose tolerance status. In contrast, ISSI-2 decreased and AUC(gluc) increased across ascending tertiles of PTH (P = .06 and P = .002, respectively). Indeed, the prevalence of GDM progressively increased from the first (22.6%) to second (25.8%) to third (33.5%) tertile of PTH (P < .001). On logistic regression analyses, the third tertile of PTH was independently associated with GDM (adjusted OR = 1.82; 95% CI, 1.09-3.02; P = .022), whereas vitamin D deficiency and insufficiency were not significant predictors of GDM. CONCLUSIONS: Increased PTH, rather than vitamin D deficiency/insufficiency, is independently associated with dysglycemia in pregnancy.
CONTEXT: Previous studies have yielded conflicting findings on the relationship between vitamin Ddeficiency/insufficiency and gestational diabetes mellitus (GDM). We hypothesized that PTH may be an underlying factor relevant to this potential association. OBJECTIVE: This study sought to evaluate the effect of vitamin D and PTH status on insulin sensitivity, β-cell function, and glycemia in pregnancy. SETTING AND DESIGN: Five-hundred-twenty-four women underwent a glucose challenge test (GCT) and oral glucose tolerance test (OGTT) in late second/early third trimester. The GCT/OGTT identified 142 women with GDM, 94 with gestational impaired glucose tolerance, 163 with an abnormal GCT and normal OGTT, and 125 with normal GCT and OGTT. MAIN OUTCOMES: Glycemia was assessed by glucose tolerance status and area under the glucose curve (AUC(gluc)) on the OGTT. Insulin sensitivity and β-cell function were assessed by Matsuda index and Insulin Secretion-Sensitivity Index-2 (ISSI-2), respectively. RESULTS: There were 166 women (31.7%) with vitamin D deficiency (25-OH-D < 50 nmol/L), 178 (34%) with insufficiency (25-OH-D ≥ 50 nmol/L and < 75 nmol/L), and 180 (34.3%) with sufficiency (25-OH-D ≥ 75 nmol/L). Vitamin D status was not associated with Matsuda index, ISSI-2, AUC(gluc), or glucose tolerance status. In contrast, ISSI-2 decreased and AUC(gluc) increased across ascending tertiles of PTH (P = .06 and P = .002, respectively). Indeed, the prevalence of GDM progressively increased from the first (22.6%) to second (25.8%) to third (33.5%) tertile of PTH (P < .001). On logistic regression analyses, the third tertile of PTH was independently associated with GDM (adjusted OR = 1.82; 95% CI, 1.09-3.02; P = .022), whereas vitamin Ddeficiency and insufficiency were not significant predictors of GDM. CONCLUSIONS: Increased PTH, rather than vitamin Ddeficiency/insufficiency, is independently associated with dysglycemia in pregnancy.