• Animal Bioscience
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• v.35 no.6
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• pp.847-857
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• 2022

Objective: The effects of maternal undernutrition during midgestation on muscle fiber histology, myosin heavy chain (MyHC) expression, methylation modification of myogenic factors, and the mammalian target of rapamycin (mTOR) signaling pathway in the skeletal muscles of prenatal and postnatal goats were examined. Methods: Twenty-four pregnant goats were assigned to a control (100% of the nutrients requirement, n = 12) or a restricted group (60% of the nutrients requirement, n = 12) between 45 and 100 days of gestation. Descendants were harvested at day 100 of gestation and at day 90 after birth to collect the femoris muscle tissue. Results: Maternal undernutrition increased (p<0.05) the fiber area of the vastus muscle in the fetuses and enhanced (p<0.01) the proportions of MyHCI and MyHCIIA fibers in offspring, while the proportion of MyHCIIX fibers was decreased (p<0.01). DNA methylation at the +530 cytosine-guanine dinucleotide (CpG) site of the myogenic factor 5 (MYF5) promoter in restricted fetuses was increased (p<0.05), but the methylation of the MYF5 gene at the +274,280 CpG site and of the myogenic differentiation (MYOD) gene at the +252 CpG site in restricted kids was reduced (p<0.05). mTOR protein signals were down-regulated (p<0.05) in the restricted offspring. Conclusion: Maternal undernutrition altered the muscle fiber type in offspring, but its relationship with methylation in the promoter regions of myogenic genes needs to be elucidated.

• Korean Journal of Agricultural Science
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• v.43 no.1
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• pp.72-79
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• 2016

It has long been known that nutritional and environmental influences during the early developmental period affect the biological mechanisms which determine animal metabolism. This phenomenon, termed 'metabolic imprinting', can cause subtle but long-lasting responses to prenatal and postnatal nutrition and even be passed onto the next generation. A large amount of research data shows that nutrient availability, in terms of quantity as well as quality, during the early developing stages can decrease the number of newborn piglets and their body weight and increase their susceptibility to death before weaning. However, investigation of potential mechanisms of 'the metabolic imprinting' effect have been scant. Therefore, it remains unknown which factors are responsible for embryonic and early postnatal nutrition and which factors are major determinants of body weight and number of new born piglets. Intrauterine undernutrition, for example, was studied using a rat model providing dams 50% restricted nutrients during pregnancy and the results showed significant decreases in birth weight of newborns. This response may be a characteristic of a subset of modulations in embryonic development which is caused by the metabolic imprinting. Underlying mechanisms of intrauterine undernutrition and growth retardation can be explained in part by epigenetics. Epigenetics modulate animal phenotypes without changes in DNA sequences. Epigenetic modifications include DNA methylation, chromatin modification and small non-coding RNA-associated gene silencing. Precise mechanisms must be identified at the morphologic, cellular, and molecular levels by using interdisciplinary nutrigenomics approaches to increase pig production. Experimental approaches for explaining these potential mechanisms will be discussed in this review.

• Animal Bioscience
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• v.35 no.7
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• pp.989-998
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• 2022

Objective: This study investigated the effects of intrauterine growth restriction (IUGR) during late pregnancy on the cell growth, proliferation, and differentiation in ovine fetal thymuses. Methods: Eighteen time-mated Mongolian ewes with singleton fetuses were allocated to three groups at d 90 of pregnancy: restricted group 1 (RG1, 0.18 MJ ME/body weight [BW]^0.75/d, n = 6), restricted group 2 (RG2, 0.33 MJ ME/BW^0.75/d, n = 6) and control group (CG, ad libitum, 0.67 MJ ME/BW^0.75/d, n = 6). Fetuses were recovered at slaughter on d 140. Results: The G0/G1 phase cell number in fetal thymus of the RG1 group was increased but the proliferation index and the expression of proliferating cell nuclear antigen (PCNA) were reduced compared with the CG group (p<0.05). Fetuses in the RG1 group exhibited decreased growth hormone receptor (GHR), insulin-like growth factor 2 receptor (IGF-2R), and their mRNA expressions (p<0.05). For the RG2 fetuses, there were no differences in the proliferation index and PCNA expression (p>0.05), but growth hormone (GH) and the mRNA expression of GHR were lower than those of the CG group (p<0.05). The thymic mRNA expressions of cyclin-dependent protein kinases (CDKs including CDK1, CDK2, and CDK4), CCNE, E2-factors (E2F1, E2F2, and E2F5) were reduced in the RG1 and RG2 groups (p<0.05), and decreased mRNA expressions of E2F4, CCNA, CCNB, and CCND were occurred in the RG1 fetuses (p<0.05). The decreased E-cadherin (E-cad) as a marker for epithelial-mesenchymal transition (EMT) was found in the RG1 and RG2 groups (p<0.05), but the OB-cadherin which is a marker for activated fibroblasts was increased in fetal thymus of the RG1 group (p<0.05). Conclusion: These results indicate that weakened GH/IGF signaling system repressed the cell cycle progression in G0/G1 phase in IUGR fetal thymus, but the switch from reduced E-cad to increased OB-cadherin suggests that transdifferentiation process of EMT associated with fibrogenesis was strengthened. The impaired cell growth, retarded proliferation and modified differentiation were responsible for impaired maturation of IUGR fetal thymus.