Perinatal Iron Deficiency Combined with a High-Fat Diet Causes Obesity and Cardiovascular Dysregulation

Author:

Bourque Stephane L.1,Komolova Marina2,McCabe Kristin2,Adams Michael A.2,Nakatsu Kanji2

Affiliation:

1. Department of Obstetrics and Gynecology (S.L.B.), University of Alberta, Edmonton, Alberta, Canada T6G 2S2

2. Department of Biomedical and Molecular Sciences (M.K., K.M., M.A.A., K.N.), Queen's University, Kingston, Ontario, Canada K7L 3N6

Abstract

Consumption of a high-fat Western diet (WD) and the resultant obesity is linked to a number of chronic pathologies, including cardiovascular dysregulation. The purpose of the present study was to determine whether perinatal iron deficiency (PID) added to the consumption of a WD would precipitate an obese phenotype with exacerbated metabolic and cardiovascular outcomes in adult offspring. Female Sprague Dawley rats were fed either a control (225 mg/kg Fe) or an iron-restricted diet (3–10 mg/kg Fe) prior to and throughout gestation. At birth, all dams were fed an iron-replete diet. At weaning, offspring were fed a normal diet or WD for up to 21 wk. Hemodynamics and locomotor activity were assessed by radiotelemetry starting at 15 wk of age. Iron restriction during pregnancy caused severe anemia in dams and offspring, resulting in 15% lower birth weights in the offspring. PID offspring fed the WD had greater caloric intake and exhibited reduced locomotor activity compared with their normal diet-fed littermates; no such effects were observed in normal iron control offspring. Despite having a similar effect on serum lipid profiles, consumption of the WD had a greater impact on body weight in the PID group, and this weight gain was due largely to visceral adipose tissue accumulation. A significant correlation between visceral adipose tissue weight and mean arterial pressure was observed in the PID offspring but not in controls. These observations demonstrate that PID predisposes offspring to an enhanced response to WD characterized by increased fat accumulation and cardiovascular dysregulation.

Publisher

The Endocrine Society

Subject

Endocrinology

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