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大鼠暴食样美味食物摄入会减少孤束核中的前胰高血糖素原。

Binge-like palatable food intake in rats reduces preproglucagon in the nucleus tractus solitarius.

机构信息

Psychology, University at Buffalo, State University of New York, Buffalo, NY 14260, USA.

Biological Sciences, University at Buffalo, State University of New York, Buffalo, NY 14260, USA.

出版信息

Physiol Behav. 2020 May 15;219:112830. doi: 10.1016/j.physbeh.2020.112830. Epub 2020 Feb 13.

DOI:10.1016/j.physbeh.2020.112830
PMID:32061682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7108972/
Abstract

Binge eating involves eating larger than normal quantities of food within a discrete period of time. The neurohormonal controls governing binge-like palatable food intake are not well understood. Glucagon-like peptide-1 (GLP-1), a hormone produced peripherally in the intestine and centrally in the nucleus tractus solitarius (NTS), reduces food intake. Given that the NTS plays a critical role in integrating peripheral and central signals relevant for food intake, as well as the role of GLP-1 in motivated feeding, we tested the hypothesis that expression of the GLP-1 precursor preproglucagon (PPG) would be reduced in the NTS of rats with a history of binge-like palatable food intake. Adult male rats received access to fat for 1 h shortly before lights off, either every day (Daily, D) or only 3d/week (Intermittent, INT). INT rats ate significantly more fat than did D rats in sessions where all rats had fat access. After ~8.5 weeks of diet maintenance, we measured plasma GLP-1 as well as NTS PPG and GLP-1 receptor expression. INT rats had significantly lower NTS PPG mRNA expression compared to D rats. However, plasma GLP-1 was significantly increased in the INT group versus D rats. No significant differences were observed in NTS GLP-1 receptor expression. We also measured plasma insulin levels, fasted blood glucose, and plasma corticosterone but no differences were detected between groups. These results support the hypothesis that binge-like eating reduces NTS GLP-1 expression, and furthermore, demonstrate divergent impacts of binge-like eating on peripheral (plasma) versus central GLP-1.

摘要

暴食症涉及在一段特定时间内摄入大于正常量的食物。控制暴食样美味食物摄入的神经激素控制机制尚不清楚。胰高血糖素样肽-1(GLP-1)是一种在肠道外周和孤束核(NTS)中枢产生的激素,可减少食物摄入。鉴于 NTS 在整合与食物摄入相关的外周和中枢信号方面发挥着关键作用,以及 GLP-1 在动机性喂养中的作用,我们假设在有暴食样美味食物摄入史的大鼠的 NTS 中,GLP-1 前体前胰高血糖素(PPG)的表达会减少。成年雄性大鼠在熄灯前不久有 1 小时的时间可以进食脂肪,每天(每日,D)或每周仅 3 天(间歇,INT)。在所有大鼠都有脂肪摄入的情况下,INT 大鼠在会议上的进食量明显多于 D 大鼠。在维持饮食约 8.5 周后,我们测量了血浆 GLP-1 以及 NTS PPG 和 GLP-1 受体表达。与 D 大鼠相比,INT 大鼠的 NTS PPG mRNA 表达明显降低。然而,INT 组的血浆 GLP-1 水平明显高于 D 组。在 NTS GLP-1 受体表达方面未观察到显著差异。我们还测量了血浆胰岛素水平、空腹血糖和血浆皮质酮,但在组间未检测到差异。这些结果支持了暴食样进食会降低 NTS GLP-1 表达的假设,并且进一步表明暴食样进食对周围(血浆)与中枢 GLP-1 的影响不同。

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本文引用的文献

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Reduced Sensory-Evoked Locus Coeruleus-Norepinephrine Neural Activity in Female Rats With a History of Dietary-Induced Binge Eating.有饮食诱导暴饮暴食史的雌性大鼠中感觉诱发的蓝斑-去甲肾上腺素神经活动减少。
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Combined Amylin/GLP-1 pharmacotherapy to promote and sustain long-lasting weight loss.联合使用胰淀素/GLP-1 药物疗法以促进和维持长期体重减轻。
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Processes and pathways to binge eating: development of an integrated cognitive and behavioural model of binge eating.暴饮暴食的过程与途径:暴饮暴食综合认知与行为模型的构建
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Preproglucagon Neurons in the Nucleus of the Solitary Tract Are the Main Source of Brain GLP-1, Mediate Stress-Induced Hypophagia, and Limit Unusually Large Intakes of Food.孤束核中的前胰高血糖素神经元是脑 GLP-1 的主要来源,介导应激引起的摄食量减少,并限制异常大量的食物摄入。
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