Early life influences on obesity risk: maternal overnutrition and programming of obesity

Abstract

While adult lifestyle factors undoubtedly contribute to the incidence of obesity and its attendant disorders, mounting evidence suggests that programming of obesity may occur following over-nutrition during development. As hypothalamic control of appetite and energy expenditure is set early in life and can be perturbed by certain exposures, such as undernutrition and altered metabolic and hormonal signals, in utero exposure to maternal obesity-related changes may contribute to programming of obesity in offspring. Data from animal studies indicate both intrauterine and postnatal environments are critical determinants of the development of pathways regulating energy homeostasis. This review summarizes recent evidence of the impact of maternal obesity on subsequent obesity risk, paying particular attention to the hypothalamic regulation of appetite and markers of metabolic control. The extraordinary rise in the rates of maternal obesity underlines an urgent need to investigate the mechanisms contributing to its transgenerational effects.

Keywords::

• appetite
• fetal
• gestation
• hypothalamus
• intrauterine
• obesity
• programming
• rat

Acknowledgements

The author acknowledges the research contributions of staff and students in her laboratory: H Chen, MJ Hansen, J Maniam, SF Ng, JM Pavia, L Prior, S Rajia and E Velkoska.

Financial and competing interests

This work was supported by a Project Grant of the National Health and Medical Research Council of Australia to MJ Morris (299875). The author has 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.

Notes

The activity of these CNS pathways is regulated by peripherally derived anorexigenic (leptin, insulin, cholecsystokinin, GLP-1, Peptide YY) signals, as well as the stomach-derived orexigenic hormone ghrelin.