Serotonin Signaling for Appetite Regulation(Panel Discussion/Molecular Mechanisms of Obesity and Eating Disorders)

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  • Nonogaki Katsunori
    Center of Excellence, Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine

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  • セロトニンシグナルと食欲調節機構(パネルディスカッション : 肥満・摂食障害の分子機構,2006年,第47回日本心身医学会総会(東京))
  • セロトニンシグナルと食欲調節機構
  • セロトニン シグナル ト ショクヨク チョウセツ キコウ

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Serotonin (5-hydroxytryptamine ; 5-HT) 2C receptors and the downstream melanocortin pathway are suggested to mediate the appetite-suppressing effects of 5-HT drugs such as m-chlorophenylpiperazine (mCPP) and fenfluramine. Here, we report that fluvoxamine, a selective serotonin reuptake inhibitor (SSRI), in the presence of SB242084, a selective 5-HT2C receptor antagonist, exerts appetite-suppressing effects while fluvoxamine or SB242084 alone has no effect. On the other hand, milnacipran, a selective serotonin (5-hydroxytryptamine ; 5-HT) and noradrenalin (NA) reuptake inhibitor, systemic administration of milnacipran significantly suppressed food intake after fasting in mice. Neither SB242084 nor SB224289, a selective 5-HT1B receptor antagonist, reversed the appetite suppressing effects of milnacipran. Moreover, milnacipran significantly increased hypothalamic pro-opiomelanocortin (POMC) and cocaineand amphetamine-regulated transcript (CART) mRNA levels. Interestingly, milnacipran did not increase plasma corticosterone and blood glucose levels, whereas fenfluramine significantly increased plasma corticosterone and blood glucose levels in association with increased hypothalamic CRH mRNA levels. These results suggest that milnacipran induces appetite suppressing effects independent of 5-HT2C and 5-HT1B receptors, whereas fluvoxamine and 5-HT2C receptor inactivation induce appetite-suppressing effects in mice. Thus, mechanisms by which SSRI and SNRI induce appetite-suppressing effects are different from those of fenfluramine.

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