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Article Dans Une Revue Domestic Animal Endocrinology Année : 2017

Moderate high or low maternal protein diets change gene expression but not the phenotype of skeletal muscle from porcine fetuses

Résumé

The aim of our study was to characterize the immediate phenotypic and adaptive regulatory responses of fetuses to different in utero conditions reflecting inadequate maternal protein supply during gestation. The gilts fed high- (250% above control) or low- (50% under control) protein diets isoenergetically adjusted at the expense of carbohydrates from the day of insemination until the fetuses were collected at day 64 or 94 of gestation. We analyzed body composition, histomorphology, biochemistry, and messenger RNA (mRNA) expression of fetal skeletal muscle. Both diets had only marginal effects on body composition and muscular cellularity of fetuses including an unchanged total number of myofibers. However, mRNA expression of myogenic regulatory factors (MYOG, MRF4, P ≤ 0.1), IGF system (IGF1, IGF1R, P ≤ 0.05) and myostatin antagonist FST (P = 0.6, in males only) was reduced in the fetal muscle exposed to a maternal low-protein diet. As a result of excess protein, MYOD, MYOG, IGF1R, and IGFBP5 mRNA expression (P ≤ 0.05) was upregulated in fetal muscle. Differences in muscular mRNA expression indicate in utero regulatory adaptive responses to maternal diet. Modulation of gene expression immediately contributes to the maintenance of an appropriate fetal phenotype that would be similar to that observed in the control fetuses. Moreover, we suggest that the modified gene expression in fetal skeletal muscle can be viewed as the origin of developmental muscular plasticity involved in the concept of fetal programming.
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hal-02628467 , version 1 (26-05-2020)

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C. Kalbe, D. Lösel, J. Block, Louis Lefaucheur, K.-P. Brüssow, et al.. Moderate high or low maternal protein diets change gene expression but not the phenotype of skeletal muscle from porcine fetuses. Domestic Animal Endocrinology, 2017, 58, pp.63-75. ⟨10.1016/j.domaniend.2016.08.003⟩. ⟨hal-02628467⟩
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