Does the maternal micronutrient deficiency (copper or zinc or vitamin E) modulate the expression of placental 11 beta hydroxysteroid dehydrogenase-2 per se predispose offspring to insulin resistance and hypertension in later life?

The relevance of maternal macronutrient deficiency on developmental origin of health and adult disorders has been well studied but not that of micronutrients. We hypothesized that chronic maternal dietary mineral (copper or zinc) or vitamin E restriction modulates the expression of placental 11 beta hydroxysteroid dehydrogenase-2 (11 beta HSD-2) per se predisposing the offspring to insulin resistance (IR) and hypertension in later life. Female weaning Swiss albino mice received a control or a 50% of Vitamin-E or Zn or Cu restricted diet and mated with control males. Pups born to the dams on the restricted diet had significantly (P < 0.001) reduced body weight and crown rump length. These offsprings were weaned on to the restricted diet till postnatal day 180. Glucose intolerance in association with hyperinsulinemeia (IR), hyperlipidemeia and increased systolic blood pressure were recorded in all the offsprings of micronutrient restricted groups. Placental 11 beta HSD-2 expression was attenuated, while activities of glucocorticoid -insensitive enzymes were unchanged in all the restricted groups. Thus, the present study reiterates the importance of micronutrients during pregnancy because chronic maternal micronutrient deficiency may alter placental 11 beta HSD-2 expression and predispose the offspring to IR and hypertension in later life.