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1 Joslin Diabetes Center, Boston, MA, USA; Gastroenterology Division, Beth Israel Medical Center, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA, USA
2 Joslin Diabetes Center, Boston, MA, USA; Division of Endocrinology, Beth Israel Medical Center, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA, USA
3 Joslin Diabetes Center, Boston, MA, USA
4 Joslin Diabetes Center, Boston, MA, USA; Division of Endocrinology, Beth Israel Medical Center, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: emaratos{at}bidmc.harvard.edu.
Genetics and environment contribute to the development of obesity, both in humans and in rodents. However the potential interaction between genes important in energy balance, strain background and dietary environment has been only minimally explored. We investigated the effects of genetic ablation of melanin-concentrating hormone (MCH), a neuropeptide with a key role in energy balance, with chow and high fat diet (HFD) in two different mouse strains, one obesity prone (C57BL/6) and the other obesity resistant (129). Substantial differences were seen in WT animals of different strains. 129 animals had significantly lower levels of spontaneous locomotor activity than C57BL/6, however 129 mice gained less weight on both chow and HFD. In both strains, deletion of MCH led to attenuated weight gain compared to WT counterparts, an effect secondary to increased energy expenditure. In both strains feeding HFD led to further increases in energy expenditure in both WT and MCH-KO mice, however this increase was more pronounced in 129 mice. In addition, mice lacking MCH have a phenotype of increased locomotor activity, an effect also seen in both strains. The relative increase in activity in MCH-/- mice is modest in animals fed chow but increases substantially when animals are placed on HFD. These studies reinforce the important role of MCH in energy homeostasis and indicate that MCH is a plausible target for anti-obesity therapy.
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