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首页> 外文期刊>American Journal of Physiology >Milnacipran, a serotonin and norepinephrine reuptake inhibitor, induces appetite-suppressing effects without inducing hypothalamic stress responses in mice.
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Milnacipran, a serotonin and norepinephrine reuptake inhibitor, induces appetite-suppressing effects without inducing hypothalamic stress responses in mice.

机译：Milnacipran是5-羟色胺和去甲肾上腺素再摄取抑制剂，可诱导食欲抑制作用，而不会引起小鼠下丘脑应激反应。

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Milnacipran, a selective serotonin (5-HT) and norepinephrine (NE) reuptake inhibitor, increases extracellular 5-HT and NA levels equally in the central nervous system. Here, we report that systemic administration of milnacipran (20-60 mg/kg) significantly suppressed food intake after fasting in C57BL6J mice. The appetite-suppressing effects of milnacipran were sustained for 5 h. Neither SB242084, a selective 5-HT2C receptor antagonist, nor SB224289, a selective 5-HT1B receptor antagonist, reversed the appetite-suppressing effects of milnacipran. Milnacipran suppressed food intake and body weight in wild-type mice and in A(y) mice, which have ectopic expression of the agouti protein. Moreover, milnacipran significantly increased hypothalamic proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) mRNA levels, while having no effect on hypothalamic neuropeptide Y, ghrelin, corticotropin-releasing hormone (CRH), and suppressor of cytokine signaling-3 mRNA levels. Interestingly,milnacipran did not increase plasma corticosterone and blood glucose levels, whereas fenfluramine, which inhibits 5-HT reuptake and stimulates 5-HT release, significantly increased plasma corticosterone and blood glucose levels in association with increased hypothalamic CRH mRNA levels. The appetite-suppressing effects of milnacipran had no effects on food intake in food-restricted, wild-type mice and A(y) mice. On the other hand, fenfluramine suppressed food intake in food-restricted wild-type mice, but it had no effects in food-restricted A(y) mice. These results suggest that inhibition of 5-HT and NA reuptake induces appetite-suppressing effects independent of 5-HT2C and 5-HT1B receptors, and increases hypothalamic POMC and CART gene expression without increasing plasma corticosterone and blood glucose levels in mice.
机译：Milnacipran是一种选择性5-羟色胺（5-HT）和去甲肾上腺素（NE）的再摄取抑制剂，可在中枢神经系统中平均提高细胞外5-HT和NA水平。在这里，我们报道了在C57BL6J小鼠禁食后，米那普仑（20-60 mg / kg）的全身给药显着抑制了食物摄入。米那普仑的食欲抑制作用持续5小时。选择性的5-HT2C受体拮抗剂SB242084和选择性的5-HT1B受体拮抗剂SB224289均未逆转米那普仑的食欲抑制作用。 Milnacipran抑制野生型小鼠和A（y）小鼠的食物摄取和体重，这些小鼠具有刺骨蛋白的异位表达。此外，米那普仑可显着增加下丘脑原卟啉黑皮质素（POMC）和可卡因和苯丙胺调节的转录（CART）mRNA水平，而对下丘脑神经肽Y，生长素释放肽，促肾上腺皮质激素释放激素（CRH）和细胞因子信号转导抑制因子3没有影响mRNA水平。有趣的是，米那普仑不增加血浆皮质酮和血糖水平，而抑制5-HT再摄取并刺激5-HT释放的芬氟拉明与下丘脑​​CRH mRNA水平升高显着增加血浆皮质酮和血糖水平。米那普仑的食欲抑制作用对食物限制的野生型小鼠和A（y）小鼠的食物摄入没有影响。另一方面，芬氟拉明抑制了限制食物的野生型小鼠的食物摄入，但对限制食物的A（y）小鼠没有影响。这些结果表明，抑制5-HT和NA再摄取可独立于5-HT2C和5-HT1B受体而抑制食欲，并增加下丘脑POMC和CART基因的表达，而不会增加小鼠血浆皮质酮和血糖水平。

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