Research Briefing Notes

Context of research

Metabolic syndrome is a serious and disturbingly common problem in Western Society. It is a complex series of morbidities (hypertension, obesity, dyslipidaemia and Type II diabetes) that contribute to a substantial proportion of early deaths in Scotland.

Substantial evidence exists to show that, at least partly, susceptibility is increased by an inappropriate maternal diet while the offspring is in utero.

What problem is our research addressing?

• Recent research suggests that the maternal environment during pregnancy can play a major part in “programming” risk of disease.

• Anaemia during pregnancy is common, even in developed countries.

• We are testing the hypothesis that maternal iron deficiency during pregnancy can predispose the infant to hypertension and obesity as an adult.

What are the potential deliverables from this research?

• Identification of critical windows of sensitivity – early, rather than late, pregnancy.

• Public health recommendations for iron supplementation during pregnancy.
  

• Identification of possible intrauterine mechanisms of fetal programming.

• Identification of gatekeeper genes and pathways for fetal programming.

Key References

Andersen HS, Gambling L, Holtrop G & McArdle HJ (2006) Maternal iron deficiency identifies critical windows for growth and cardiovascular development in the rat postimplantation embryo. J Nutr 136, 1171-1177.

Bayele HK, McArdle HJ & Srai SKS (2006) cis and trans regulation of hepcidin expression by upstream regulatory factor. Blood E-pub DOI 10.1182.

Gambling L, Dunford S, Wallace DI, Zuur G, Solanky N, Srai SKS & McArdle HJ (2003) Iron deficiency during pregnancy affects post-natal blood pressure in the rat. J. Physiol. 552, 603-610.

Jones HN, Ashworth CJ, Page KR & McArdle HJ (2006a) Cortisol stimulates System A amino acid transport and SNAT2 expression in a human placental cell line (BeWo). Am. J. Physiol. 291, E596-603.

Jones HN, Ashworth CJ, Page KR & McArdle HJ (2006b) Expression and adaptive regulation of amino acid transport system A in a placental cell line under amino acid restriction. Reprod. 131, 591-560.