Katherine A Bowers1, Sjurdur F Olsen2, Wei Bao3, Thorhallur I Halldorsson4, Marin Strøm5, Cuilin Zhang6. 1. Division of Biostatistics and Epidemiology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH; katherine.bowers@cchmc.org zhangcu@mail.nih.gov. 2. Centre for Fetal Programming, Department of Epidemiology Research, Statens Serum Institute, Copenhagen, Denmark; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA; 3. Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Rockville, MD; Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, IA; 4. Centre for Fetal Programming, Department of Epidemiology Research, Statens Serum Institute, Copenhagen, Denmark; Faculty of Food Science and Nutrition, University of Iceland, Raykjavik, Iceland; and. 5. Centre for Fetal Programming, Department of Epidemiology Research, Statens Serum Institute, Copenhagen, Denmark; Faculty of Natural and Health Sciences, University of the Faroe Islands, Tórshavn, Faroe Islands. 6. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA; katherine.bowers@cchmc.org zhangcu@mail.nih.gov.
Abstract
BACKGROUND: Evidence from experimental studies has demonstrated that higher than normal iron concentrations can lead to pancreatic β cell dysfunction and impaired glucose metabolism. Studies on body iron stores in early pregnancy and subsequent gestational diabetes mellitus (GDM) risk are sparse. OBJECTIVE: Our objective was to determine whether biomarkers of body iron stores measured in early pregnancy are associated with GDM risk. METHODS: A case-control study of 350 GDM cases and 349 non-GDM controls was conducted in participants from the Danish National Birth Cohort. Blood was collected at a mean ± SD gestational age of 9.4 ± 3.2 wk. Plasma biomarkers of iron stores, including ferritin and soluble transferrin receptor (sTfR), were measured. Logistic regression was used to estimate the OR of GDM associated with quintiles of plasma biomarkers of body iron stores, controlling for maternal age, family history of diabetes, exercise in pregnancy, parity, and prepregnancy body mass index (BMI). RESULTS: Cases were older (mean ± SD age: 32.2 ± 4.3 compared with 29.9 ± 4.2 y) and had a higher BMI (in kg/m(2); mean ± SD: 28.7 ± 6.0 compared with 24.1 ± 4.6) than controls. Plasma concentrations of both ferritin and sTfR in early pregnancy were significantly higher in GDM cases than in controls [means ± SDs: 80.6 ± 56.0 compared with 71.8 ± 50.1 μg/L (P = 0.03) and 1.5 ± 0.7 compared with 1.4 ± 0.6 mg/L (P = 0.002) for ferritin and sTfR, respectively]. Ferritin was positively and significantly associated with GDM risk even after adjustment for major risk factors of GDM, including prepregnancy BMI. ORs across increasing quintiles of ferritin were 1.00 (reference), 1.25 (95% CI: 0.70, 2.22), 1.89 (95% CI: 1.06, 3.37), 0.82 (95% CI: 0.46, 1.48), and 2.34 (95% CI: 1.30, 4.21) (P-linear trend = 0.02). CONCLUSION: These findings suggest that plasma ferritin measured in early pregnancy is significantly and positively associated with GDM risk.
BACKGROUND: Evidence from experimental studies has demonstrated that higher than normal iron concentrations can lead to pancreatic β cell dysfunction and impaired glucose metabolism. Studies on body iron stores in early pregnancy and subsequent gestational diabetes mellitus (GDM) risk are sparse. OBJECTIVE: Our objective was to determine whether biomarkers of body iron stores measured in early pregnancy are associated with GDM risk. METHODS: A case-control study of 350 GDM cases and 349 non-GDM controls was conducted in participants from the Danish National Birth Cohort. Blood was collected at a mean ± SD gestational age of 9.4 ± 3.2 wk. Plasma biomarkers of iron stores, including ferritin and soluble transferrin receptor (sTfR), were measured. Logistic regression was used to estimate the OR of GDM associated with quintiles of plasma biomarkers of body iron stores, controlling for maternal age, family history of diabetes, exercise in pregnancy, parity, and prepregnancy body mass index (BMI). RESULTS: Cases were older (mean ± SD age: 32.2 ± 4.3 compared with 29.9 ± 4.2 y) and had a higher BMI (in kg/m(2); mean ± SD: 28.7 ± 6.0 compared with 24.1 ± 4.6) than controls. Plasma concentrations of both ferritin and sTfR in early pregnancy were significantly higher in GDM cases than in controls [means ± SDs: 80.6 ± 56.0 compared with 71.8 ± 50.1 μg/L (P = 0.03) and 1.5 ± 0.7 compared with 1.4 ± 0.6 mg/L (P = 0.002) for ferritin and sTfR, respectively]. Ferritin was positively and significantly associated with GDM risk even after adjustment for major risk factors of GDM, including prepregnancy BMI. ORs across increasing quintiles of ferritin were 1.00 (reference), 1.25 (95% CI: 0.70, 2.22), 1.89 (95% CI: 1.06, 3.37), 0.82 (95% CI: 0.46, 1.48), and 2.34 (95% CI: 1.30, 4.21) (P-linear trend = 0.02). CONCLUSION: These findings suggest that plasma ferritin measured in early pregnancy is significantly and positively associated with GDM risk.
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