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肠道-大脑多巴胺轴:热量摄入的调节系统。

The gut-brain dopamine axis: a regulatory system for caloric intake.

机构信息

The John B Pierce Laboratory, New Haven, CT 06519, USA.

出版信息

Physiol Behav. 2012 Jun 6;106(3):394-9. doi: 10.1016/j.physbeh.2012.02.026. Epub 2012 Mar 3.

DOI:10.1016/j.physbeh.2012.02.026
PMID:22406348
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3348418/
Abstract

Post-ingestive factors are known to strongly modulate feeding behavior by providing feedback signals to the central nervous system on the current physiological state of the organism. Of particular interest is the identification of the physiological pathways that permit the brain to sense post-ingestive signals. We will review recent evidence supporting the concept that direct stimulation of the gastrointestinal tract with nutrients induces release of the catecholamine neurotransmitter dopamine. In addition, changes in dopamine efflux produced by direct stimulation of the gastrointestinal tract were found to reflect the caloric load of the infusates, suggesting that dopamine signaling may function as a central caloric sensor that mediates adjustments in intake according to the caloric density of a meal. Consistent with the above, blockade of dopamine signaling disrupts flavor-nutrient associations and impairs the regulatory capacity to maintain constant caloric intake during intra-gastric feeding. Future research must determine the exact pathways linking gut nutrient administration to dopamine efflux. Current evidence points to parallel contributions by pre- and post-absorptive pathways, indicating that dopamine systems constitute a site of convergence through which distinct physiological signals can exert control over ingestive behaviors.

摘要

进食后因素通过向中枢神经系统提供关于机体当前生理状态的反馈信号,强烈调节进食行为。特别感兴趣的是确定允许大脑感知进食后信号的生理途径。我们将回顾最近的证据,支持以下观点,即直接刺激胃肠道的营养素会诱导儿茶酚胺神经递质多巴胺的释放。此外,发现直接刺激胃肠道引起的多巴胺外流量变化反映了输注物的热量负荷,表明多巴胺信号可能作为中央热量传感器,根据膳食的热量密度调节摄入。与上述观点一致,阻断多巴胺信号会破坏味道-营养的关联,并损害在胃内喂养期间维持恒定热量摄入的调节能力。未来的研究必须确定将肠道营养素管理与多巴胺外排联系起来的确切途径。目前的证据表明,吸收前和吸收后途径的平行贡献,表明多巴胺系统构成了一个汇聚点,通过该汇聚点,不同的生理信号可以控制摄食行为。

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本文引用的文献

1
Regulation of fat intake in the absence of flavour signalling.在没有味道信号的情况下调节脂肪摄入。
J Physiol. 2012 Feb 15;590(4):953-72. doi: 10.1113/jphysiol.2011.218289. Epub 2012 Jan 4.
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Up-regulation of intestinal type 1 taste receptor 3 and sodium glucose luminal transporter-1 expression and increased sucrose intake in mice lacking gut microbiota.肠道 1 型味觉受体 3 和钠-葡萄糖共转运蛋白-1 表达上调,以及缺乏肠道微生物群的小鼠蔗糖摄入量增加。
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Gut fat sensing in the negative feedback control of energy balance--recent advances.肠道脂肪感应在能量平衡的负反馈控制中的作用——最新进展。
Physiol Behav. 2011 Sep 26;104(4):621-3. doi: 10.1016/j.physbeh.2011.05.003. Epub 2011 May 6.
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Selective deletion of the leptin receptor in dopamine neurons produces anxiogenic-like behavior and increases dopaminergic activity in amygdala.选择性敲除多巴胺神经元中的瘦素受体可产生焦虑样行为,并增加杏仁核中的多巴胺能活性。
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Addict Biol. 2012 Jan;17(1):95-107. doi: 10.1111/j.1369-1600.2010.00294.x. Epub 2011 Feb 11.
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Participation of hindbrain AMP-activated protein kinase in glucoprivic feeding.后脑 AMP 激活蛋白激酶在糖饥饿进食中的作用。
Diabetes. 2011 Feb;60(2):436-42. doi: 10.2337/db10-0352.
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Proc Natl Acad Sci U S A. 2011 Feb 1;108(5):2094-9. doi: 10.1073/pnas.1011508108. Epub 2011 Jan 18.
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Gut T1R3 sweet taste receptors do not mediate sucrose-conditioned flavor preferences in mice.肠道 T1R3 甜味受体并不介导小鼠对蔗糖条件性口味偏好。
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