Hypothalamic neuroendocrine circuitry is programmed by maternal obesity: interaction with postnatal nutritional
Hui Chen1, David Simar, Margaret J Morris
1Department of Pharmacology, School of Medical Sciences, University of New South Wales, New South Wales, Australia.
Plos One
|July 17, 2009
Summary
Maternal obesity and post-weaning high-fat diets synergistically promote offspring obesity and metabolic dysfunction through distinct neuroendocrine pathways, highlighting critical early life nutrition impacts.
Area of Science:
- Endocrinology and Metabolism
- Neuroscience
- Developmental Biology
Background:
- Early life nutrition significantly influences hypothalamic development and energy homeostasis.
- Maternal overnutrition programs appetite-regulating neurons (NPY, POMC) in offspring.
- Long-term effects of early programming and interaction with post-weaning diet remain unclear.
Purpose of the Study:
- To investigate the long-term effects of maternal obesity and postnatal overnutrition on offspring metabolism.
- To examine the interaction between maternal diet, litter size, and post-weaning high-fat diet (HFD) on offspring metabolic programming.
- To elucidate the neuroendocrine mechanisms underlying diet-induced obesity in offspring.
Main Methods:
- Female Sprague Dawley rats were fed chow or HFD pre-mating, during gestation, and lactation.
- Postnatal overnutrition induced by litter size reduction (3/litter vs. 12/litter).
- Offspring were weaned onto chow or HFD for 15 weeks; hypothalamic regulators and metabolic markers were analyzed.
Main Results:
- Offspring from obese dams exhibited increased weight gain irrespective of post-weaning diet.
- Maternal obesity combined with post-weaning HFD exacerbated hyperphagia, adiposity, hyperlipidemia, and glucose intolerance.
- These metabolic disturbances were associated with enhanced hypothalamic neuropeptide Y (NPY) signaling and leptin resistance.
- Litter size reduction negatively impacted insulin and adiponectin, while suppressing NPY/POMC mRNA despite normal energy intake.
Conclusions:
- Maternal obesity, litter size, and post-weaning HFD induce offspring obesity through distinct neuroendocrine mechanisms.
- Additive effects of maternal obesity and post-weaning HFD significantly amplify metabolic disorders in offspring.
- Early life nutritional interventions are crucial for preventing long-term metabolic consequences.
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