Mechanisms mediating the impact of maternal obesity on offspring hypothalamic development and later function
Isadora C Furigo1, Laura Dearden2
1Centre for Sport, Exercise and Life Sciences, School of Life Sciences, Coventry University, Coventry, United Kingdom.
Insights
Maternal obesity during pregnancy can permanently alter offspring
Area of Science:
- Neuroscience
- Developmental Biology
- Endocrinology
Background:
- Rising global obesity rates complicate pregnancies.
- Maternal obesity poses risks for mother and child, including long-term health issues like obesity, diabetes, and cardiovascular disease.
- Offspring exposed to maternal obesity show increased food intake, suggesting altered neuronal control of appetite.
Purpose of the Study:
- To review hypothalamic development.
- To examine how maternal obesity impacts offspring hypothalamic structure and function.
- To identify factors in an obese in utero environment that may cause permanent hypothalamic changes.
Main Methods:
- Literature review of studies on maternal obesity and offspring neurodevelopment.
- Analysis of animal models investigating hypothalamic development and function.
- Examination of metabolic hormone roles (leptin, ghrelin, insulin) in hypothalamic plasticity.
Main Results:
- The hypothalamus, crucial for energy homeostasis, is sensitive to metabolic signals.
- Maternal obesity can disrupt hypothalamic development and function in offspring.
- Specific factors within the obese in utero environment mediate lasting changes.
Conclusions:
- Maternal obesity during pregnancy can lead to lasting structural and functional changes in the offspring's hypothalamus.
- These hypothalamic alterations may contribute to increased long-term risks of metabolic diseases in offspring.
- Understanding these mechanisms is vital for preventing intergenerational obesity and related disorders.
Abstract:
As obesity rates have risen around the world, so to have pregnancies complicated by maternal obesity. Obesity during pregnancy is not only associated with negative health outcomes for the mother and the baby during pregnancy and birth, there is also strong evidence that exposure to maternal obesity causes an increased risk to develop obesity, diabetes and cardiovascular disease later in life. Animal models have demonstrated that increased weight gain in offspring exposed to maternal obesity is usually preceded by increased food intake, implicating altered neuronal control of food intake as a likely area of change. The hypothalamus is the primary site in the brain for maintaining energy homeostasis, which it coordinates by sensing whole body nutrient status and appropriately adjusting parameters including food intake. The development of the hypothalamus is plastic and regulated by metabolic hormones such as leptin, ghrelin and insulin, making it vulnerable to disruption in an obese in utero environment. This review will summarise how the hypothalamus develops, how maternal obesity impacts on structure and function of the hypothalamus in the offspring, and the factors that are altered in an obese in utero environment that may mediate the permanent changes to hypothalamic function in exposed individuals.
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