Abstract
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.
Highlights
Placental insufficiency and various other maternal factors, such as environmental stress, disease, and malnutrition, contribute to intrauterine growth retardation (IUGR)during gestation, which results in impaired fetal development and decreased bodyweight (BW) at birth [1]
IUGR, called fetal growth restriction (FGR), which leads to stunting of postnatal growth and decreased nutrient utilization efficiency in the offspring, adversely affects the whole-body composition and results in prolonged disruption of homeostasis as it predisposes the fetus to metabolic disorders, such as insulin resistance [1,2]
This study aimed to elucidate the effect of maternal undernutrition (MUN) on fetal skeletal muscle metabolism that links to the retardation of the fetal muscle development in Japanese Black cows
Summary
Placental insufficiency and various other maternal factors, such as environmental stress, disease, and malnutrition, contribute to intrauterine growth retardation (IUGR)during gestation, which results in impaired fetal development and decreased bodyweight (BW) at birth [1]. Affects the whole-body composition and results in prolonged disruption of homeostasis as it predisposes the fetus to metabolic disorders, such as insulin resistance [1,2]. Maternal undernutrition (MUN) is one of the major factors that contribute to the induction of IUGR. Previous studies have reported that MUN impairs the growth and metabolism of fetal organs, including the skeletal muscle and liver [3,4,5,6,7,8], by altering the secretion and/or sensitivity of glucose, insulin, and insulin-like growth factor-1 (IGF1) [8]. MUN-induced impairment of skeletal muscle growth and metabolism adversely affect fetal metabolism by modulating whole-body insulin sensitivity and glucose homeostasis [9]
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