Longitudinal Analysis of the Interaction Between Obesity and Pregnancy on Iron Homeostasis: Role of Hepcidin.

Autor: Flores-Quijano ME; Departamento de Nutrición y Bioprogramación, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Ciudad de México, México., Montalvo-Velarde I; Unidad de Investigación Médica en Nutrición, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social (IMSS), Ciudad de México, México., Vital-Reyes VS; Hospital de Obstetricia y Ginecología #3, Centro Médico La Raza, IMSS, Ciudad de México, México., Rodríguez-Cruz M; Unidad de Investigación Médica en Nutrición, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social (IMSS), Ciudad de México, México., Rendón-Macías ME; Unidad de Investigación en Epidemiología, Centro Médico Nacional Siglo XXI, IMSS, Ciudad de México, México., López-Alarcón M; Unidad de Investigación Médica en Nutrición, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social (IMSS), Ciudad de México, México. Electronic address: marsau2@prodigy.net.mx.
Jazyk: angličtina
Zdroj: Archives of medical research [Arch Med Res] 2016 Oct; Vol. 47 (7), pp. 550-556.
DOI: 10.1016/j.arcmed.2016.11.011
Abstrakt: Background and Aims: When pregnancy occurs in obese women, two opposite mechanisms for iron homeostasis concur: increased need for available iron to support erythropoiesis and decreased iron mobilization from diets and stores due to obesity-related inflammation linked to overexpressed hepcidin. Few studies have examined the role of hepcidin on maternal iron homeostasis in the context of obese pregnancy. The aim of the study was to evaluate the combined effect of maternal obesity and pregnancy on hepcidin and maternal iron status while accounting for inflammation and iron supplementation.
Methods: We conducted a secondary analysis of a cohort of pregnant women recruited from a referral obstetric hospital in Mexico City. Circulating biomarkers of iron status (hepcidin, ferritin [SF], transferrin receptor [sTfR], erythropoietin [EPO]), and inflammation (C-reactive protein [CRP], tumor necrosis factor-[TNF]α, and interleukin-[IL]6) were determined monthly throughout pregnancy. Repeated measures ANOVA and logistic regression models were used for statistics.
Results: Twenty-three obese (Ob) and 25 lean (Lc) women were studied. SF and hepcidin declined, and EPO and sTfR increased throughout pregnancy in both groups. sTfR increased more in Ob than in Lc (p = 0.024). The smallest hepcidin decline occurred in iron-supplemented Ob women compared to non-supplemented Lc women (p = 0.022). The risk for iron deficiency at the end of pregnancy was higher for Ob than for Lc (OR = 4.45, 95% CI = 2.07-9.58) after adjusting for iron supplementation and hepcidin concentration.
Conclusion: Pre-gestational obesity increases the risk of maternal iron deficiency despite iron supplementation. Overexpressed hepcidin appears to be a potential mechanism.
(Copyright © 2016 IMSS. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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