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White and Brown Adipose Grafts: An Approach to Correct Reproductive, Metabolic, and Renal Deficits in Black and Tan Brachyury (BTBR) Obese Mice
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Birthweight phenotype genotype mismatch in cardiometabolic programming.

Lars Meinertz Byg1,2, Carol A Wang1,2, Roger Smith1,2,3

  • 1University of Newcastle, School of Medicine afnd Public Health, Newcastle, NSW, Australia.

Communications Medicine
|June 19, 2026
PubMed
Summary
This summary is machine-generated.

A mismatch between genetic predisposition and actual birth weight in early life is linked to increased cardiometabolic risk factors like central adiposity and insulin resistance in adulthood. This finding supports the Barker hypothesis regarding fetal growth programming adult disease.

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Area of Science:

  • Developmental origins of health and disease (DOHaD)
  • Genetics and epigenetics of cardiometabolic risk
  • Perinatal programming of adult health

Background:

  • The Barker hypothesis posits that poor fetal growth programs adult cardiometabolic disease.
  • Genetic studies suggest pleiotropic effects of birth weight genetics on cardiometabolic risk, challenging the Barker hypothesis.
  • This study investigates if genetic influences on birth weight interact with the observed birth weight phenotype.

Purpose of the Study:

  • To examine the interplay between birth weight genetics and birth weight phenotype in relation to adult cardiometabolic health.
  • To determine if a mismatch between genetic potential and phenotypic birth weight influences cardiometabolic risk factors.
  • To re-evaluate the Barker hypothesis in light of genetic and phenotypic data.

Main Methods:

  • A cohort of 1167 offspring was followed from mid-pregnancy to age 27.
  • Repeated measures of body mass index, insulin resistance, LDL cholesterol, and systolic blood pressure were collected.
  • Linear mixed-effects models assessed associations between birth weight polygenic scores and cardiometabolic outcomes, stratified by high vs. low birth weight phenotype.

Main Results:

  • A birth weight phenotype-genotype mismatch was associated with increased central adiposity and insulin resistance in young adults.
  • Fetuses with low phenotypic birth weight but high birth weight polygenic scores showed increased central adiposity and insulin resistance.
  • Individuals with high phenotypic birth weight but low birth weight polygenic scores also showed increased insulin resistance, but no effect was observed on LDL cholesterol or systolic blood pressure.

Conclusions:

  • Deviation from fetal growth potential, rather than absolute birth weight, underlies the relationship with adult disease risk.
  • These findings support the Barker hypothesis, emphasizing the importance of fetal growth trajectory.
  • Identifying individuals with a birth weight phenotype-genotype mismatch may enable early risk prediction for future cardiometabolic diseases.