Abstract
Maternal obesity is a major risk factor for the subsequent development of obesity and Type 2 diabetes in the child. This relationship appears to be driven largely by the exposure of the fetus to an increased nutrient supply during critical periods of development, which results in persistent changes in the structure and function of key systems involved in the regulation of energy balance, appetite and fat deposition. One of the key targets is the fat cell, or adipocyte, in which prenatal overnutrition programs a heightened capacity for fat storage. The increasing prevalence of maternal obesity has led to an urgent need for strategies to break the resulting intergenerational cycle of obesity and metabolic disease. This review will discuss the relationship between maternal obesity and poor metabolic health of the offspring, with a particular focus on the involvement of adipose tissue, recent clinical studies examining potential strategies for intervention and priority areas for further research.
Financial & competing interests disclosure
BS Muhlhausler is supported by a Career Development Award from the National Health and Medical Research Council of Australia (NHMRC). MA Vithayathil is a graduate student whose scholarship is supported by an Australian Postgraduate Award. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
Maternal obesity is a major risk factor for obesity and associated metabolic disorders in the child.
The association between maternal obesity and obesity in the child is a result of an increased nutrient supply to the fetus during critical periods of development.
The fat cell is a key target of this developmental programming, and exposure to an increased nutrient supply before birth prematurely ‘switches on’ key genes in adipose tissue that are responsible for lipid storage, resulting in an increased propensity for fat accumulation after birth.
The increase in fat storage places the individual at increased risk of obesity and associated comorbidities.
These effects are not easily reversible – therefore, early intervention is essential.
In humans, the major period of fat cell development begins before birth and extends into the first year of life.
Exposure to an increased nutrient supply during this period is an important determinant of fat cell size and number and the capacity of individuals for storing fat throughout the life course.
Current research is focused on potential nutritional interventions to improve outcomes in infants born to overweight/obese mothers, but few results have been published to date.
There is an urgent need to accelerate this research and to also focus on mechanistic studies in humans.
The next 5 years is likely to see a move toward the development of specific guidelines for the nutritional management of overweight/obese mothers and their infants.