期刊
CELL METABOLISM
卷 6, 期 5, 页码 398-405出版社
CELL PRESS
DOI: 10.1016/j.cmet.2007.10.008
关键词
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资金
- Medical Research Council [G0600717B] Funding Source: researchfish
- NIDDK NIH HHS [R21 DK068330, R01 DK065171, P30 DK072476, P01 DK56116, P01 DK056116] Funding Source: Medline
- NIMH NIH HHS [R01 MH61583, R01 MH061583] Funding Source: Medline
- Wellcome Trust [081713] Funding Source: Medline
The burden of type 2 diabetes and its associated premature morbidity and mortality is rapidly growing, and the need for novel efficacious treatments is pressing. We report here that serotonin 2C receptor (5-HT2CR) agonists, typically investigated for their anorectic properties, significantly improve glucose tolerance and reduce plasma insulin in murine models of obesity and type 2 diabetes. Importantly, 5-HT2CR agonist-induced improvements in glucose homeostasis occurred at concentrations of agonist that had no effect on ingestive behavior, energy expenditure, locomotor activity, body weight, or fat mass. We determined that this primary effect on glucose homeostasis requires downstream activation of melanocortin-4 receptors (MC4Rs), but not MC3Rs. These findings suggest that pharmacological targeting of 5-HT(2C)Rs may enhance glucose tolerance independently of alterations in body weight and that this may prove an effective and mechanistically novel strategy in the treatment of type 2 diabetes.
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