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Maternal obesity as a risk factor for developing diabetes in offspring: An epigenetic point of view. | LitMetric

Maternal obesity as a risk factor for developing diabetes in offspring: An epigenetic point of view.

World J Diabetes

University of Lille, EA4489, Maternal Malnutrition and Programming of Metabolic Diseases, Lille 59000, France.

Published: April 2021

AI Article Synopsis

  • The developmental origin of health and disease concept suggests that early development factors, particularly maternal obesity and rapid growth at birth, significantly influence the risk of age-related diseases like overweight and type 2 diabetes.
  • These early life conditions affect adipose tissue and pancreatic β-cell programming, leading to unhealthy fat cells, inflammation, and reduced insulin production, which may persist into adulthood.
  • Recent rodent studies highlight the role of epigenetic changes stemming from maternal nutrition that can affect offspring and contribute to a hereditary risk for type 2 diabetes, emphasizing the long-term health impacts of early development.

Article Abstract

According to the developmental origin of health and disease concept, the risk of many age-related diseases is not only determined by genetic and adult lifestyle factors but also by factors acting during early development. In particular, maternal obesity and neonatal accelerated growth predispose offspring to overweight and type 2 diabetes (T2D) in adulthood. This concept mainly relies on the developmental plasticity of adipose tissue and pancreatic β-cell programming in response to suboptimal during the perinatal period. These changes result in unhealthy hypertrophic adipocytes with decreased capacity to store fat, low-grade inflammation and loss of insulin-producing pancreatic β-cells. Over the past years, many efforts have been made to understand how maternal obesity induces long-lasting adipose tissue and pancreatic β-cell dysfunction in offspring and what are the molecular basis of the transgenerational inheritance of T2D. In particular, rodent studies have shed light on the role of epigenetic mechanisms in linking maternal nutritional manipulations to the risk for T2D in adulthood. In this review, we discuss epigenetic adipocyte and β-cell remodeling during development in the progeny of obese mothers and the persistence of these marks as a basis of obesity and T2D predisposition.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8040079PMC
http://dx.doi.org/10.4239/wjd.v12.i4.366DOI Listing

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