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Epidemiological studies have shown that maternal undernutrition during pregnancy (MU) leads to intrauterine growth retardation and low birth weight and may predispose individuals to the development of metabolic syndrome symptoms later in life such as overweight. Some clues from a model of prenatal maternal 70% food-restricted diet throughout gestation in pregnant female rats (FR30) suggest that the white adipose tissue (WAT) is a key target of MU fetal programming. Under standard diet, although showing a lean phenotype, adult FR30 male rats were predisposed to adiposity exhibiting higher serum leptin and corticosterone concentration, two hormones actively involved in WAT regulation. Although FR30 procedure does not worsen the metabolic syndrome features induced by HF diet, FR30HF rats gained more weight and showed hyperleptinemia suggesting increased adiposity. WAT FR30 adult rats revealed marked changes in transcript levels of several genes. In particular, leptin and Ob-Rb, many peptide precursors and receptors, factors involved in lipogenesis and glucocorticoid sensitivity mRNA expression levels as well as mechanisms involved in leptin sensitivity, were modified in FR30 offspring in depot-specific and diet-specific manners. These modifications might predispose for altered fat accumulation in adult male rat offspring. [ABSTRACT FROM AUTHOR]

Several studies have shown that maternal undernutrition leading to low birth weight predisposes offspring to the development of metabolic pathologies such as obesity. Using a model of prenatal maternal 70% food restriction diet (FR30) in rat, we evaluated whether postweaning high-fat (HF) diet would amplify the phenotype observed under standard diet. We investigated biological parameters as well as gene expression profile focusing on white adipose tissues (WAT) of adult offspring. FR30 procedure does not worsen the metabolic syndrome features induced by HF diet. However, FR30HF rats displayed catch-up growth to match the body weight of adult control HF animals, suggesting an increase of adiposity while showing hyperleptinemia and a blunted increase of corticosterone. Using quantitative RT-PCR array, we demonstrated that FR30HF rats exhibited leptin and Ob-Rb as well as many peptide precursor and receptor gene expression variations in WAT. We also showed that the expression of genes involved in adipogenesis was modified in FR30HF animals in a depot-specific manner. We observed an opposite variation of STAT3 phosphorylation levels, suggesting that leptin sensitivity is modified in WAT adult FR30 offspring. We demonstrated that 11β-HSD1, 11β-HSD2, GR, and MR genes are coexpressed in WAT and that FR30 procedure modifies gene expression levels, especially under HF diet. In particular, level variation of 11β-HSD2, whose protein expression was detected by Western blotting, may represent a novel mechanism that may affect WAT glucocorticoid sensitivity. Data suggest that maternal undernutrition differently programs the adult offspring WAT gene expression profile that may predispose for altered fat deposition. [ABSTRACT FROM AUTHOR]