Why the study?
Mechanisms underlying maternal undernutrition-induced fetal skeletal muscle growth impairment in cattle remained to be elucidated.
Does maternal undernutrition alter amino acid metabolism and gene expression in fetal calf muscle?
Does maternal undernutrition alter amino acid metabolism and gene expression in fetal calf muscle?
Maternal undernutrition alters amino acid levels and downregulates genes associated with energy expenditure, glucose homeostasis, and angiogenesis in fetal calf muscle.
This is the authors' abstract. We don't add key points for this paper.
To elucidate the mechanisms underlying maternal undernutrition (MUN)-induced fetal skeletal muscle growth impairment in cattle, the longissimus thoracis muscle of Japanese Black fetal calves at 8.5 months in utero was analyzed by an integrative approach with metabolomics and transcriptomics. The pregnant cows were fed on 60% (low-nutrition, LN) or 120% (high-nutrition, HN) of their overall nutritional requirement during gestation. MUN markedly decreased the bodyweight and muscle weight of the fetus. The levels of amino acids (AAs) and arginine-related metabolites including glutamine, gamma-aminobutyric acid (GABA), and putrescine were higher in the LN group than those in the HN group. Metabolite set enrichment analysis revealed that the highly different metabolites were associated with the metabolic pathways of pyrimidine, glutathione, and AAs such as arginine and glutamate, suggesting that MUN resulted in AA accumulation rather than protein accumulation. The mRNA expression levels of energy metabolism-associated genes, such as PRKAA1, ANGPTL4, APLNR, CPT1B, NOS2, NOS3, UCP2, and glycolytic genes were lower in the LN group than in the HN group. The gene ontology/pathway analysis revealed that the downregulated genes in the LN group were associated with glucose metabolism, angiogenesis, HIF-1 signaling, PI3K-Akt signaling, pentose phosphate, and insulin signaling pathways. Thus, MUN altered the levels of AAs and expression of genes associated with energy expenditure, glucose homeostasis, and angiogenesis in the fetal muscle.
Maternal undernutrition effects in fetal calves are hypothesis-generating; leaves open translational relevance to human fetal programming and requires validation.
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Muroya et al. (2021) studied this question.
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