Epigenetics and Nutrition: Molecular Mechanisms and Tissue Adaptation in Developmental Programming

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Molecular Mechanisms in Nutritional Epigenetics

Abstract

Biological mechanisms regulating normal growth, development, and nutrient utilization are programmed in utero for postnatal growth and adult function. An increasing body of evidence shows that epigenetic mechanisms drive developmental programming. Among the factors that underlie developmental programming, most studies have focused on maternal nutrition during critical developmental windows. Critical periods include the time surrounding conception, placentation, and organogenesis. Imbalances of key nutrients or other environmental factors can potentially leave epigenetic marks in the genome that can be carried forward through subsequent developmental stages and likely across generations. In this chapter, we address the complex interplay between nutrition, epigenomics, and physiological response to explore the impact of parental nutrition during the periconceptual period and throughout gestation on fetal organ development and metabolism. We will primarily focus on the development of both the hepatic and muscular systems of livestock species; however, relevant findings from human and animal models will also be integrated. The complex and intricate relationships among nutrition, epigenetics, and developmental programming warrant further exploration to fully dissect its mechanisms and implications.

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Abbreviations

Akt:

Ak strain transforming (a serine/threonine protein kinase)

ATP:

Adenosine triphosphate

B2:

Vitamin B2, riboflavin

B6:

Vitamin B6, pyridoxine

B12:

Vitamin B12, cobalamin

IGF:

Insulin-like growth factor

IGF-1:

Insulin-like growth factor one

IGF2:

Insulin-like growth factor two

LG:

Low gain

LP:

Low protein

MG:

Moderate gain

miRNAs:

MicroRNAs

mTOR:

Mammalian target of rapamycin

NADPH:

Nicotinamide adenine dinucleotide phosphate

NoVTM:

No supplementation of vitamin and mineral

OCM:

One-carbon metabolism

PAG:

Pregnancy-associated glycoproteins

PI3K:

Phosphoinositide 3 kinase

SAH:

S-adenosylhomocysteine

SAM:

S-adenosylmethionine

VEGFA-receptor 1:

Vascular endothelial growth factor receptor-1

VTM:

Vitamin and mineral supplemented

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Acknowledgments

The authors would like to thank our colleagues, including undergraduate and graduate students and postdoctoral fellows for their dedication. We also thank the many laboratory and farm personnel who have made such important contributions to these efforts. We are also thankful to the various sources of funding, including the North Dakota Agricultural Experiment Station (NDAES), the North Dakota State Board of Agricultural Research and Education (SBARE), the Agriculture and Food Research Initiative of the USDA’s National Institute of Food and Agriculture, and Purina Animal Nutrition LLC, Gray Summit, MO, USA. W.J.S.D. was financially supported by the Agricultural Research Service, US Department of Agriculture, under Agreement No. 58-6010-1-005, by the Alabama Agricultural Experiment Station—Hatch program of the National Institute of Food and Agriculture, US Department of Agriculture.

Mention of a trade name, proprietary product, or specific agreement does not constitute a guarantee or warranty by the USDA and does not imply approval to the inclusion of other products that may be suitable. USDA is an equal opportunity provider and employer.

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Correspondence to Wellison J. S. Diniz .

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The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as potential conflicts of interest.

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This chapter contains no studies with human/animal participants performed by authors.

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© 2024 The Author(s), under exclusive license to Springer Nature Switzerland AG

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Diniz, W.J.S. et al. (2024). Epigenetics and Nutrition: Molecular Mechanisms and Tissue Adaptation in Developmental Programming. In: Vaschetto, L.M. (eds) Molecular Mechanisms in Nutritional Epigenetics. Epigenetics and Human Health, vol 12. Springer, Cham. https://doi.org/10.1007/978-3-031-54215-2_4

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