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限制喂养/补充方案对大鼠 NPY 和 POMC 的影响,但对 5-羟色胺转运体无影响。

Changes in NPY and POMC, but not serotonin transporter, following a restricted feeding/repletion protocol in rats.

机构信息

Unidad de Cartografía Cerebral, Instituto Pluridisciplinar, Universidad Complutense de Madrid, 28040 Madrid, Spain.

出版信息

Brain Res. 2010 Feb 8;1313:103-12. doi: 10.1016/j.brainres.2009.11.075. Epub 2009 Dec 5.

DOI:10.1016/j.brainres.2009.11.075
PMID:19968967
Abstract

Serotonin (5-HT) plays a key role in controlling food intake and feeding behaviour and drugs targeting the 5-HT transporter (SERT) at the synaptic cleft have been used to treat feeding related disorders. To test the hypothesis that SERT might be one of the etiologic factors in the rebound hyperphagia that frequently follows the abandoning of calorie restriction diets, brain SERT content and gene expression were assessed in a restricted feeding/repletion (RFR) protocol in female rats. Animals were food-restricted (2 h access to food per day) for 7 consecutive days and then allowed constant free access to food (FAF). This intermittent fasting protocol resulted in rebound hyperphagia. Higher levels of plasma corticosterone during fasting in food-deprived rats were used as an index of hypothalamic-pituitary-adrenal axis activation. Neither brain SERT density nor expression was modified following the RFR protocol. Nevertheless, with respect to other messengers involved in eating behaviour, in the presence of low plasma leptin levels, an increase in NPY expression and a parallel decrease in POMC expression were observed in the hypothalamic arcuate nucleus of rats killed just before rebound hyperphagia. Food-restricted animals provide a tool for the further study of neurochemical alterations and for the development of new drugs to treat alterations that may occur in humans when dieting is abandoned.

摘要

血清素(5-HT)在控制食物摄入和进食行为方面起着关键作用,靶向突触间隙 5-羟色胺转运体(SERT)的药物已被用于治疗与进食相关的疾病。为了测试 SERT 可能是经常跟随热量限制饮食放弃后反弹性暴食的一个病因因素的假说,在雌性大鼠的限时喂养/补充(RFR)方案中评估了脑 SERT 含量和基因表达。动物连续 7 天每天接受 2 小时的食物限制,然后允许自由获得食物(FAF)。这种间歇性禁食方案导致了暴食反弹。在禁食期间,食物剥夺大鼠的血浆皮质酮水平升高被用作下丘脑-垂体-肾上腺轴激活的指标。在 RFR 方案后,脑 SERT 密度或表达均未发生改变。然而,与参与进食行为的其他信使相比,在低血浆瘦素水平下,在暴食反弹之前被杀死的大鼠下丘脑弓状核中观察到 NPY 表达增加和 POMC 表达平行下降。限制食物的动物为进一步研究神经化学变化和开发新药物提供了工具,以治疗人类在节食时可能发生的变化。

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