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Mice with MCH ablation resist diet-induced obesity through strain-specific mechanisms.
Am J Physiol Regul Integr Comp Physiol. 2005 Jul; 289(1):R117-24.AJ

Abstract

Genetics and environment contribute to the development of obesity, in both humans and 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 a 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 wild-type (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 with WT counterparts, an effect secondary to increased energy expenditure. In both strains, feeding a 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 antiobesity therapy.

Authors+Show Affiliations

Joslin Diabetes Center, Boston, Massachusetts, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15731402

Citation

Kokkotou, Efi, et al. "Mice With MCH Ablation Resist Diet-induced Obesity Through Strain-specific Mechanisms." American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, vol. 289, no. 1, 2005, pp. R117-24.
Kokkotou E, Jeon JY, Wang X, et al. Mice with MCH ablation resist diet-induced obesity through strain-specific mechanisms. Am J Physiol Regul Integr Comp Physiol. 2005;289(1):R117-24.
Kokkotou, E., Jeon, J. Y., Wang, X., Marino, F. E., Carlson, M., Trombly, D. J., & Maratos-Flier, E. (2005). Mice with MCH ablation resist diet-induced obesity through strain-specific mechanisms. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 289(1), R117-24.
Kokkotou E, et al. Mice With MCH Ablation Resist Diet-induced Obesity Through Strain-specific Mechanisms. Am J Physiol Regul Integr Comp Physiol. 2005;289(1):R117-24. PubMed PMID: 15731402.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mice with MCH ablation resist diet-induced obesity through strain-specific mechanisms. AU - Kokkotou,Efi, AU - Jeon,Justin Y, AU - Wang,Xiaomei, AU - Marino,Francis E, AU - Carlson,Michael, AU - Trombly,Daniel J, AU - Maratos-Flier,Eleftheria, Y1 - 2005/02/24/ PY - 2005/2/26/pubmed PY - 2005/7/14/medline PY - 2005/2/26/entrez SP - R117 EP - 24 JF - American journal of physiology. Regulatory, integrative and comparative physiology JO - Am. J. Physiol. Regul. Integr. Comp. Physiol. VL - 289 IS - 1 N2 - Genetics and environment contribute to the development of obesity, in both humans and 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 a 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 wild-type (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 with WT counterparts, an effect secondary to increased energy expenditure. In both strains, feeding a 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 antiobesity therapy. SN - 0363-6119 UR - https://www.unboundmedicine.com/medline/citation/15731402/Mice_with_MCH_ablation_resist_diet_induced_obesity_through_strain_specific_mechanisms_ L2 - http://www.physiology.org/doi/full/10.1152/ajpregu.00861.2004?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -