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高脂肪饮食诱导的肥胖和胰岛素抵抗的特征是边缘皮质基底神经节回路的β振荡信号的差异。

High-fat diet-induced obesity and insulin resistance are characterized by differential beta oscillatory signaling of the limbic cortico-basal ganglia loop.

机构信息

Charité University Medicine Berlin, Department of Endocrinology and Metabolism, Berlin, Germany.

Center for Cardiovascular Research - Charité-Universitätsmedizin Berlin, Berlin, Germany.

出版信息

Sci Rep. 2017 Nov 14;7(1):15555. doi: 10.1038/s41598-017-15872-x.

Abstract

The concept of brain circuit disorders has been proposed for a variety of neuropsychiatric diseases, characterized by pathological disturbances of neuronal networks including changes in oscillatory signaling of re-entrant cortico-subcortical loops in the basal ganglia system. Parts of this circuitry play a pivotal role in energy homeostasis. We therefore investigated whether high-fat diet (HFD) induced obesity is associated with changes in oscillatory signaling in the limbic cortico-basal ganglia loop. We performed multi-site in-vivo electrophysiological recordings of local field potentials within this network under urethane anesthesia in adult rats after 4 weeks of HFD feeding compared to age-matched controls. Recordings were performed at baseline and during systemic glucose challenge. Our analysis demonstrates increased oscillatory beta power in the nucleus accumbens (NAC) associated with decreased beta coherence between cortex and NAC in animals fed a HFD. Spontaneous beta oscillatory power strongly correlated with endocrine markers of obesity. The glucose challenge increased beta oscillations in control animals but not in animals receiving the HFD. Furthermore direct intracerebroventricular insulin injection increased beta oscillations in the NAC. The present study provides evidence for aberrant oscillatory signaling in the limbic cortico-basal ganglia loop that might contribute to the dysfunctional information processing in obesity.

摘要

脑回路紊乱的概念已经被提出用于各种神经精神疾病,其特征是神经元网络的病理性紊乱,包括基底神经节系统中回旋皮质-皮质下回路的振荡信号变化。该电路的部分区域在能量平衡中起着关键作用。因此,我们研究了高脂肪饮食(HFD)诱导的肥胖是否与边缘皮质-基底神经节回路中振荡信号的变化有关。我们在成年大鼠接受 HFD 喂养 4 周后,在麻醉状态下,在多个部位对该网络内的局部场电位进行了活体电生理记录,并与年龄匹配的对照组进行了比较。记录在基线和全身葡萄糖挑战期间进行。我们的分析表明,HFD 喂养的动物的伏隔核(NAC)中β波功率增加,而皮层和 NAC 之间的β波相干性降低。自发β振荡功率与肥胖的内分泌标志物强烈相关。葡萄糖挑战增加了对照组动物的β振荡,但接受 HFD 的动物没有增加。此外,直接向侧脑室注射胰岛素可增加 NAC 中的β振荡。本研究提供了边缘皮质-基底神经节回路中异常振荡信号的证据,这可能导致肥胖症中信息处理功能障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2298/5686216/4396f84cc57a/41598_2017_15872_Fig1_HTML.jpg

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