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Heisler LK Jobst EE Sutton GM Zhou L Borok E Thornton-Jones Z Liu HY Zigman JM Balthasar N Kishi T Lee CE Aschkenasi CJ Zhang CY Yu J Boss O Mountjoy KG Clifton PG Lowell BB Friedman JM Horvath T Butler AA Elmquist JK Cowley MA 《Neuron》2006,51(2):239-249
The neural pathways through which central serotonergic systems regulate food intake and body weight remain to be fully elucidated. We report that serotonin, via action at serotonin1B receptors (5-HT1BRs), modulates the endogenous release of both agonists and antagonists of the melanocortin receptors, which are a core component of the central circuitry controlling body weight homeostasis. We also show that serotonin-induced hypophagia requires downstream activation of melanocortin 4, but not melanocortin 3, receptors. These results identify a primary mechanism underlying the serotonergic regulation of energy balance and provide an example of a centrally derived signal that reciprocally regulates melanocortin receptor agonists and antagonists in a similar manner to peripheral adiposity signals. 相似文献
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Serotonin 2C receptor agonists improve type 2 diabetes via melanocortin-4 receptor signaling pathways 总被引:3,自引:0,他引:3
Zhou L Sutton GM Rochford JJ Semple RK Lam DD Oksanen LJ Thornton-Jones ZD Clifton PG Yueh CY Evans ML McCrimmon RJ Elmquist JK Butler AA Heisler LK 《Cell metabolism》2007,6(5):398-405
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-HT(2C)R) 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-HT(2C)R 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. 相似文献
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