Parental diet, pregnancy outcomes and offspring health: metabolic determinants in developing oocytes and embryos

Kevin D. Sinclair, Adam J. Watkins

Research output: Contribution to journalArticle

Abstract

The periconceptional period, embracing the terminal stages of oocyte growth and post-fertilisation development up to implantation, is sensitive to parental nutrition. Deficiencies or excesses in a range of macro- and micronutrients during this period can lead to impairments in fertility, fetal development and long-term offspring health. Obesity and genotype-related differences in regional adiposity are associated with impaired liver function and insulin resistance, and contribute to fatty acid-mediated impairments in sperm viability and oocyte and embryo quality, all of which are associated with endoplasmic reticulum stress and compromised fertility. Disturbances to maternal protein metabolism can elevate ammonium concentrations in reproductive tissues and disturb embryo and fetal development. Associated with this are disturbances to one-carbon metabolism, which can lead to epigenetic modifications to DNA and associated proteins in offspring that are both insulin resistant and hypertensive. Many enzymes involved in epigenetic gene regulation use metabolic cosubstrates (e.g. acetyl CoA and S-adenosyl methionine) to modify DNA and associated proteins, and so act as 'metabolic sensors' providing a link between parental nutritional status and gene regulation. Separate to their genomic contribution, spermatozoa can also influence embryo development via direct interactions with the egg and by seminal plasma components that act on oviductal and uterine tissues.
Original languageEnglish
Pages (from-to)99-114
Number of pages16
JournalReproduction, fertility and development
Volume26
Issue number1
DOIs
Publication statusPublished - 5 Dec 2013

Fingerprint

pregnancy outcome
fetal development
Pregnancy Outcome
insulin resistance
epigenetics
Oocytes
embryo (animal)
oocytes
embryogenesis
Embryonic Structures
spermatozoa
uterine tissue
Diet
Epigenomics
Fertility
Spermatozoa
seminal plasma
liver function
Health
adiposity

Keywords

  • epigenetics
  • fetal programming
  • gametes
  • periconception
  • sperm

Cite this

@article{a0afe2edc1bd476dacf6583e3e018262,
title = "Parental diet, pregnancy outcomes and offspring health: metabolic determinants in developing oocytes and embryos",
abstract = "The periconceptional period, embracing the terminal stages of oocyte growth and post-fertilisation development up to implantation, is sensitive to parental nutrition. Deficiencies or excesses in a range of macro- and micronutrients during this period can lead to impairments in fertility, fetal development and long-term offspring health. Obesity and genotype-related differences in regional adiposity are associated with impaired liver function and insulin resistance, and contribute to fatty acid-mediated impairments in sperm viability and oocyte and embryo quality, all of which are associated with endoplasmic reticulum stress and compromised fertility. Disturbances to maternal protein metabolism can elevate ammonium concentrations in reproductive tissues and disturb embryo and fetal development. Associated with this are disturbances to one-carbon metabolism, which can lead to epigenetic modifications to DNA and associated proteins in offspring that are both insulin resistant and hypertensive. Many enzymes involved in epigenetic gene regulation use metabolic cosubstrates (e.g. acetyl CoA and S-adenosyl methionine) to modify DNA and associated proteins, and so act as 'metabolic sensors' providing a link between parental nutritional status and gene regulation. Separate to their genomic contribution, spermatozoa can also influence embryo development via direct interactions with the egg and by seminal plasma components that act on oviductal and uterine tissues.",
keywords = "epigenetics, fetal programming, gametes, periconception, sperm",
author = "Sinclair, {Kevin D.} and Watkins, {Adam J.}",
year = "2013",
month = "12",
day = "5",
doi = "10.1071/RD13290",
language = "English",
volume = "26",
pages = "99--114",
journal = "Reproduction, fertility and development",
issn = "1031-3613",
publisher = "CSIRO",
number = "1",

}

Parental diet, pregnancy outcomes and offspring health : metabolic determinants in developing oocytes and embryos. / Sinclair, Kevin D.; Watkins, Adam J.

In: Reproduction, fertility and development, Vol. 26, No. 1, 05.12.2013, p. 99-114.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Parental diet, pregnancy outcomes and offspring health

T2 - metabolic determinants in developing oocytes and embryos

AU - Sinclair, Kevin D.

AU - Watkins, Adam J.

PY - 2013/12/5

Y1 - 2013/12/5

N2 - The periconceptional period, embracing the terminal stages of oocyte growth and post-fertilisation development up to implantation, is sensitive to parental nutrition. Deficiencies or excesses in a range of macro- and micronutrients during this period can lead to impairments in fertility, fetal development and long-term offspring health. Obesity and genotype-related differences in regional adiposity are associated with impaired liver function and insulin resistance, and contribute to fatty acid-mediated impairments in sperm viability and oocyte and embryo quality, all of which are associated with endoplasmic reticulum stress and compromised fertility. Disturbances to maternal protein metabolism can elevate ammonium concentrations in reproductive tissues and disturb embryo and fetal development. Associated with this are disturbances to one-carbon metabolism, which can lead to epigenetic modifications to DNA and associated proteins in offspring that are both insulin resistant and hypertensive. Many enzymes involved in epigenetic gene regulation use metabolic cosubstrates (e.g. acetyl CoA and S-adenosyl methionine) to modify DNA and associated proteins, and so act as 'metabolic sensors' providing a link between parental nutritional status and gene regulation. Separate to their genomic contribution, spermatozoa can also influence embryo development via direct interactions with the egg and by seminal plasma components that act on oviductal and uterine tissues.

AB - The periconceptional period, embracing the terminal stages of oocyte growth and post-fertilisation development up to implantation, is sensitive to parental nutrition. Deficiencies or excesses in a range of macro- and micronutrients during this period can lead to impairments in fertility, fetal development and long-term offspring health. Obesity and genotype-related differences in regional adiposity are associated with impaired liver function and insulin resistance, and contribute to fatty acid-mediated impairments in sperm viability and oocyte and embryo quality, all of which are associated with endoplasmic reticulum stress and compromised fertility. Disturbances to maternal protein metabolism can elevate ammonium concentrations in reproductive tissues and disturb embryo and fetal development. Associated with this are disturbances to one-carbon metabolism, which can lead to epigenetic modifications to DNA and associated proteins in offspring that are both insulin resistant and hypertensive. Many enzymes involved in epigenetic gene regulation use metabolic cosubstrates (e.g. acetyl CoA and S-adenosyl methionine) to modify DNA and associated proteins, and so act as 'metabolic sensors' providing a link between parental nutritional status and gene regulation. Separate to their genomic contribution, spermatozoa can also influence embryo development via direct interactions with the egg and by seminal plasma components that act on oviductal and uterine tissues.

KW - epigenetics

KW - fetal programming

KW - gametes

KW - periconception

KW - sperm

UR - http://www.scopus.com/inward/record.url?scp=84889859963&partnerID=8YFLogxK

U2 - 10.1071/RD13290

DO - 10.1071/RD13290

M3 - Article

AN - SCOPUS:84889859963

VL - 26

SP - 99

EP - 114

JO - Reproduction, fertility and development

JF - Reproduction, fertility and development

SN - 1031-3613

IS - 1

ER -