Nutritional marginal zinc deficiency disrupts placental 11β-hydroxysteroid dehydrogenase type 2 modulation.

S. SUPASAI; A. M. ADAMO; Y. L. HUANG; N. W. GAIKWAD; P. I. OTEIZA; H. KUCERA; P. MATHIEU

Food and Function

Royal Society of Chemistry

Año: 2016 vol. 7 p. 84 - 92

2042-6496

This paper investigated if marginal zinc nutrition during gestation could affect fetal exposure to glucocorticoidsas a consequence of a deregulation of placental 11βHSD2 expression. Placenta 11β-hydroxysteroiddehydrogenase type 2 (11βHSD2) plays a central role as a barrier protecting the fetus from the deleteriouseffects of excess maternal glucocorticoids. Rats were fed control (25 μg zinc per g diet) or marginal (10 μgzinc per g diet, MZD) zinc diets from day 0 through day 19 (GD19) of gestation. At GD19, corticosteroneconcentration in plasma, placenta, and amniotic fluid was similar in both groups. However, protein andmRNA levels of placenta 11βHSD2 were significantly higher (25% and 58%, respectively) in MZD dams thanin controls. The main signaling cascades modulating 11βHSD2 expression were assessed. In MZD placentasthe activation of ERK1/2 and of the downstream transcription factor Egr-1 was low, while p38 phosphorylationand SP-1-DNA binding were low compared to the controls. These results point to a centralrole of ERK1/Egr-1 in the regulation of 11βHSD2 expression under the conditions of limited zinc availability.In summary, results show that an increase in placenta 11βHSD2 expression occurs as a consequenceof gestational marginal zinc nutrition. This seems to be due to a low tissue zinc-associatedderegulation of ERK1/2 rather than to exposure to high maternal glucocorticoid exposure. The deleteriouseffects on brain development caused by diet-induced marginal zinc deficiency in rats do not seem to bedue to fetal exposure to excess glucocorticoids.