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Why and How Imprinted Genes Drive Fetal Programming.

Bernard J Crespi1

  • 1Department of Biological Sciences and Human Evolutionary Studies Program, Simon Fraser University, Burnaby, BC, Canada.

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|March 3, 2020
PubMed
Summary
This summary is machine-generated.

Maternal gene biases linked to imprinted genes increase metabolic disease risk through effects on fetal growth and development. Paternal gene biases also contribute, but risks can be managed by targeting imprinted gene expression.

Keywords:
fetal programminggenomic imprintingmetabolic syndromemother-offspring conflicttype 2 diabetes

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Area of Science:

  • Genetics and Developmental Biology
  • Metabolic Disease Research

Background:

  • Imprinted genes regulate fetal and childhood growth, influencing early development.
  • Kinship theory of imprinting predictions lack integration with fetal programming and metabolic disease data.

Purpose of the Study:

  • Define paternal and maternal gene optima for early human growth.
  • Evaluate how imprinted gene expression impacts metabolic disease risk.
  • Integrate kinship theory with fetal programming and metabolic disease data.

Main Methods:

  • Review of evidence on imprinted gene effects on birth weight, body composition, growth, and development.
  • Analysis of maternal and paternal gene biases in relation to metabolic disease risk factors.
  • Application of kinship theory and mother-offspring conflict principles.

Main Results:

  • Maternal gene biases are primarily linked to metabolic disease risk via reduced placental efficacy, low birth weight, and altered body composition.
  • Paternal gene biases may contribute to metabolic disease through reduced brown fat thermiogenesis and postnatal catch-up growth.
  • Imprinted gene expression influences insulin resistance, adiposity, and early puberty.

Conclusions:

  • Metabolic disease risks are significantly influenced by imprinted gene expression, particularly maternal biases.
  • Dietary and pharmacological interventions targeting imprinted genes can alleviate disease risks.
  • Kinship theory provides a framework for future research on fetal programming and metabolic disease.