Abstract

Maternal magnesium restriction irreversibly increased body fat %, specially the visceral adiposity in WNIN rat offspring. We have now investigated whether the increased visceral adiposity was associated with increased adipogenesis and glucocorticoid stress. Female, weanling WNIN rats were fed for 12 weeks, a control (AIN 93G) diet (MgC) or the same with 70% restriction of Mg (MgR) and mated with control males. Some of the pregnant MgR dams were rehabilitated from parturition and their pups weaned on to control diet (MgRP). At weaning half of the pups from MgR dams were shifted to control diet (MgRW) while the other half continued on Mg restriction (MgR). mRNA expression for fatty acid synthase (FAS) and 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) was significantly higher in MgR adipose tissue offspring. However leptin mRNA expression was comparable among different groups. Both the rehabilitation regimes corrected the expression of 11β-HSD1 but not that of FAS. Maternal Mg restriction predisposed the offspring to increased glucocorticoid stress (11β-HSD1) that could underlie the increased body fat %/central adiposity.

Highlights

  • Adverse intrauterine environment predisposes the offspring to metabolic syndrome in adult life [1,2]

  • We recently showed that Mg restriction in utero predisposed the rat offspring to long term adiposity, specially visceral adiposity [12,13] and the offspring had increased expression of fatty acid synthase (FAS) and decreased leptin expression in adipose tissue [13]

  • The mRNA expression of fatty acid synthase was significantly increased in Mg restriction (MgR) compared to MgC offspring and this result was not corrected by either of the rehabilitation regimes (Figure 1)

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Summary

Introduction

Adverse intrauterine environment predisposes the offspring to metabolic syndrome in adult life [1,2]. We showed earlier that maternal micronutrient (mineral and vitamin) restriction in WNIN rats increased the body fat%, altered plasma lipid and insulin levels and was associated with altered oxidative stress and adipocytokine levels in offspring suggesting that micronutrients were important in developmental programming of adiposity in the offspring [3,4]. Available literature suggests that modulation of epigenetics and stress (glucocorticoid and/or oxidative) could be some common pathways involved in developmental programming for adult diseases in the offspring due to maternal malnutrition during pregnancy and/or lactation [5,6]. This study aimed to determine whether or not altered mRNA expression (transcriptional regulation) underlies the changes in 11β-HSD1, FAS and leptin expression Vis-avis visceral adiposity in the offspring of Mg restricted WNIN rat dams

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