期刊
HORMONE AND METABOLIC RESEARCH
卷 40, 期 4, 页码 257-261出版社
GEORG THIEME VERLAG KG
DOI: 10.1055/s-2008-1058064
关键词
fetal programming; corticosterone; mineralocorticoid receptor; glucocorticoid receptor; 11 beta-HSD1; 11 beta-HSD2; perinatal food restriction
Maternal undernutrition leads to intrauterine growth retardation and predisposes to the development of pathologies in adulthood. The hypothalamo-pituitary-adrenal axis is a major target of early-life programming. We showed previously that perinatal maternal 50% food restriction leads to hypothalamo-pituitary-adrenal axis hyperactivity and disturbs glucocorticoid feedback in adult male rats. To try to better understand these alterations, we studied several factors involved in corticosterone sensitivity. We showed that unlike the restricted expression of 11 beta-HSD2 mRNA, the 11 beta-HSD1, glucocorticoid, and mineralocorticorid receptor genes are widely distributed in rat. In contrast to the hypothalamus, we confirmed that maternal undernutrition modulates hippocampal corticosterone receptor balance and leads to increased 11 beta-HSD1 gene expression. In the pituitary, rats exhibited a huge increase in both mRNA and mineralocorticoid receptor binding capacities as well as decreased 11 beta-HSD1/11 beta-HSD2 gene expression. Using in situ hybridization, we showed that the mineralocorticoid receptor gene was expressed in rat corticotroph cells and by other adenopituitary cells. In the adrenal gland, maternal food restriction decreased 11 beta-HSD2 mRNA. This study demonstrated that maternal food restriction has both long-term and tissue-specific effects on gene expression of factors involved in glucocorticoid sensitivity and that it could contribute, via glucocorticoid excess, to the development of adult diseases.
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