| Autor: |
Mendoza LC; Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau, 08025 Barcelona, Spain.; CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Madrid, Spain., Harreiter J; Clinical Division of Endocrinology and Metabolism, Department of Internal Medicine III, Gender Medicine Unit, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria., Desoye G; Department of Obstetrics and Gynecology, Medical University of Graz, 8036 Graz, Austria., Simmons D; Macarthur Clinical School, School of Medicine, Western Sydney University, Campbelltown, NSE 2560, Australia., Adelantado JM; Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau, 08025 Barcelona, Spain., Kautzky-Willer A; Clinical Division of Endocrinology and Metabolism, Department of Internal Medicine III, Gender Medicine Unit, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria., Zawiejska A; Department of Reproduction, Poznan University of Medical Sciences, 60-525 Poznan, Poland., Wender-Ozegowska E; Department of Reproduction, Poznan University of Medical Sciences, 60-525 Poznan, Poland., Lapolla A; Department of Medicine, University of Padova, 35128 Padova, Italy., Dalfra MG; Department of Medicine, University of Padova, 35128 Padova, Italy., Bertolotto A; Department of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy., Devlieger R; Obstetrics and Gynecology, University Hospitals KU Leuven, 3000 Leuven, Belgium., Dunne F; College of Medicine, Nursing and Health Sciences, School of Medicine, National University of Ireland, H91 TK33 Galway, Ireland., Mathiesen ER; Center for Pregnant Women with Diabetes, Departments of Endocrinology and Obstetrics, Rigshospitalet, University of Copenhagen, DK-1165 Copenhagen, Denmark., Damm P; Center for Pregnant Women with Diabetes, Departments of Endocrinology and Obstetrics, Rigshospitalet, University of Copenhagen, DK-1165 Copenhagen, Denmark., Andersen LL; Department of Gynecology and Obstetrics, Odense University Hospital, 5000 Odense, Denmark., Jensen DM; Department of Gynecology and Obstetrics, Odense University Hospital, 5000 Odense, Denmark., Hill D; Lawson Health Research Institute, St. Joseph Health Care, London, ON N6A 4V2, Canada., van Poppel MNM; Institute of Sport Science, University of Graz, 8010 Graz, Austria., Corcoy R; Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau, 08025 Barcelona, Spain.; CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Madrid, Spain.; Departament de Medicina, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain. |
| Abstrakt: |
Studies on the relationship between vitamin D (VitD) and glucose homeostasis usually consider either total VitD or 25OHD3 but not 25OHD2 and epimers. We aimed to evaluate the cross-sectional association of VitD compounds with glucose homeostasis measurements in pregnant women with overweight/obesity participating in the Vitamin D And Lifestyle Intervention for Gestational Diabetes Mellitus Prevention study. Methods: The analysis included 912 women. Inclusion criteria: <20 weeks gestation, body mass index ≥29 kg/m2 and information on exposure and outcome variables at baseline. Measurements: A 75 g OGTT at <20, 24−28 and 35−37 weeks gestation (except if previous diabetes diagnosis). Exposure variables: 25OHD2, 25OHD3 and C3-epimer. Outcome variables: fasting and post-challenge insulin sensitivity and secretion indices, corresponding disposition indices (DI), plasma glucose at fasting and 1 and 2 h, hyperglycemia in pregnancy (HiP). Statistics: Multivariate regression analyses with adjustment. Results: Baseline VitD sufficiency was 66.3%. Overall, VitD compounds did not show strong associations with any glucose homeostasis measures. 25OHD3 showed direct significant associations with: FPG at <20 and 24−28 weeks (standardized β coefficient (β) 0.124, p = 0.030 and 0.111, p = 0.026 respectively), 2 h plasma glucose at 24−28 weeks (β 0.120, p = 0.018), and insulin sensitivity (1/HOMA-IR, β 0.127, p = 0.027) at 35−37 weeks; it showed an inverse association with fasting DI (QUCKI*HOMA-β) at <20 and 24−28 weeks (β −0.124, p = 0.045 and β −0.148, p = 0.004 respectively). 25OHD2 showed direct associations with post-challenge insulin sensitivity (Matsuda, β 0.149, p = 0.048) at 24−28 weeks) and post-challenge DI (Matsuda*Stumvoll phase 1) at 24−28 and 35−37 weeks (β 0.168, p = 0.030, β 0.239, p = 0.006). No significant association with C3-epimer was observed at any time period. Conclusions: In these women with average baseline VitD in sufficiency range, VitD compounds did not show clear beneficial associations with glucose homeostasis measures. |
