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Stimulation of melanocortin-3 receptors accelerates the satiation process and increases the α-MSH expression in high-fat diet-fed rats.
Behavioral Neuroscience ( IF 1.6 ) Pub Date : 2021-04-26 , DOI: 10.1037/bne0000468
Daniel Díaz-Urbina 1 , Rodrigo Erick Escartín-Pérez 1 , Carolina Escobar 2 , Juan Manuel Mancilla-Díaz 1 , Verónica Elsa López-Alonso 1
Affiliation  

The knowledge about the role of MC3 receptors (MC3r) in the regulation of feeding behavior is limited. The present study was conducted to determine whether MC3r mediates the hypophagic effects of the melanocortins under conditions of positive energy balance. Male Wistar rats were fed with a high-fat diet (HFD) for 15 days and on day 16 the animals received an intracerebroventricular injection of the following treatments: Vehicle, D-Trp8-γ-melanocyte-stimulating hormone (MSH; MC3r agonist), SHU9119 (MC3r/MC4r antagonist), or D-Trp8-γ-MSH+SHU9119. Food intake was measured and the behavioral satiety sequence (BSS) analysis was carried out during the first hour of the dark phase. The c-Fos and α-MSH immunoreactivity in the arcuate nucleus (ARC) was evaluated 60 min later the onset of food intake. The results indicated that D-Trp8-γ-MSH decreased the ingestion of the HFD and this effect is associated with the early development of the satiation process Moreover, the D-Trp8-γ-MSH increased the accumulation of the α-MSH in the ARC and the c-Fos activity in the PVN. The antagonist SHU9119 partially prevented the D-Trp8-γ-MSH-induced hypophagia. Moreover, behavioral analysis suggests that central activation of MC3r accelerated the cessation of feeding in conditions of positive energy balance; the possible role of MC4r is discussed. Present data indicate that central stimulation of MC3r prevented the overconsumption of the HFD without affecting the natural satiation process, suggesting a potential use of MC3r for the treatment of eating disorders that are stimulated by hypercaloric diets. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

中文翻译:

黑皮质素 3 受体的刺激加速了饱食过程并增加了高脂饮食喂养大鼠的 α-MSH 表达。

关于 MC3 受体 (MC3r) 在调节摄食行为中的作用的知识是有限的。本研究旨在确定 MC3r 是否在正能量平衡条件下介导黑皮质素的低吞噬作用。雄性 Wistar 大鼠用高脂肪饮食 (HFD) 喂养 15 天,在第 16 天,动物接受以下治疗的脑室内注射:载体,D-Trp8-γ-黑素细胞刺激素(MSH;MC3r 激动剂) 、SHU9119(MC3r/MC4r 拮抗剂)或 D-Trp8-γ-MSH+SHU9119。测量食物摄入量并在黑暗阶段的第一小时进行行为饱腹感序列 (BSS) 分析。在食物摄入开始 60 分钟后评估弓状核 (ARC) 中的 c-Fos 和 α-MSH 免疫反应性。结果表明,D-Trp8-γ-MSH 减少了 HFD 的摄入,这种作用与饱食过程的早期发展有关。此外,D-Trp8-γ-MSH 增加了 α-MSH 在ARC 和 PVN 中的 c-Fos 活性。拮抗剂 SHU9119 部分阻止了 D-Trp8-γ-MSH 诱导的食欲减退。此外,行为分析表明,MC3r 的中枢激活加速了能量正平衡条件下进食的停止;讨论了 MC4r 的可能作用。目前的数据表明,MC3r 的中枢刺激防止了 HFD 的过度消耗,而不影响自然饱食过程,这表明 MC3r 可能用于治疗由高热量饮食刺激的饮食失调。(PsycInfo 数据库记录 (c) 2021 APA,
更新日期:2021-04-28
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