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Voluntary exercise delays monogenetic obesity and overcomes reproductive dysfunction of the melanocortin-4 receptor
B G Irani1, Z Xiang, M C Moore
1Department of Medicinal Chemistry, College of Pharmacy, University of Florida, P.O. Box 100485, Gainesville, FL 32610, USA.
Abstract:
The melanocortin system is involved in hypothalamic regulation of energy homeostasis. The melanocortin-4 receptor (MC4R) has been linked to both obesity and reproductive dysfunction. Deletion of the MC4R from the mouse genome has resulted in phenotypes including adult onset obesity, hyperphagia, and difficulty in reproducing when homozygote parents are bred. Additionally, polymorphisms of the human MC4R have been identified in morbidly obese children and adults. Herein, we have identified that voluntary exercise, provided via the presence of a running wheel, impedes the monogenetic obesity (at 20 weeks of age running wheel housed body weight=31+/-1.8 g versus conventionally housed body weight=41+/-2.3 g, a 25% decrease in body weight p<0.01), hyperphagia (average cumulative food intake is not statistically different than wild type mice housed in running wheel cages), and reproductive dysfunction phenotypes associated with the MC4R knockout mice housed by conventional means. These data demonstrate the novel finding that voluntary exercise at a young age may hinder genetically induced obesity.
Insights
Voluntary exercise in young mice with a melanocortin-4 receptor (MC4R) knockout hinders genetically induced obesity and hyperphagia. Early exercise may prevent obesity phenotypes in mice lacking MC4R.
Area of Science:
- Neuroendocrinology
- Metabolic Regulation
- Genetics
Background:
- The melanocortin system regulates energy homeostasis via the hypothalamus.
- Melanocortin-4 receptor (MC4R) is implicated in obesity and reproductive issues.
- MC4R gene deletion causes obesity, overeating, and reproductive problems in mice.
Purpose of the Study:
- To investigate the impact of voluntary exercise on MC4R knockout mouse phenotypes.
- To determine if early-life exercise can mitigate genetically induced obesity.
Main Methods:
- MC4R knockout mice were housed with or without running wheels.
- Body weight and food intake were monitored.
- Reproductive function was assessed.
Main Results:
- Voluntary exercise significantly reduced body weight by 25% in MC4R knockout mice.
- Exercise normalized hyperphagia, with food intake similar to wild-type mice.
- Exercise ameliorated reproductive dysfunction phenotypes.
Conclusions:
- Voluntary exercise can counteract monogenetic obesity and related phenotypes in MC4R knockout mice.
- Early-life physical activity may be a strategy to prevent genetically driven obesity.
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