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肥胖的多模态神经影像学:从结构 - 功能机制到精准干预

Multimodal Neuroimaging of Obesity: From Structural-Functional Mechanisms to Precision Interventions.

作者信息

Liu Wenhua, Li Na, Tang Dongsheng, Qin Lang, Zhu Zhiqiang

机构信息

School of Kinesiology, Shenzhen University, Shenzhen 518000, China.

Brain Imaging Research Center, Shenzhen University, Shenzhen 518000, China.

出版信息

Brain Sci. 2025 Apr 25;15(5):446. doi: 10.3390/brainsci15050446.

DOI:10.3390/brainsci15050446
PMID:40426616
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12109827/
Abstract

PURPOSE

Obesity's metabolic consequences are well documented; however, its neurobiological underpinnings remain elusive. This systematic review addresses a critical gap by synthesizing evidence on obesity-induced neuroplasticity across structural, functional, and molecular domains through advanced neuroimaging.

METHODS

According to PRISMA guidelines, we systematically searched (2015-2024) across PubMed/Web of Science, employing MeSH terms: ("Obesity" [Majr]) AND ("Neuroimaging" [Mesh] OR "Magnetic Resonance Imaging" [Mesh]). A total of 104 studies met the inclusion criteria. The inclusion criteria required the following: (1) multimodal imaging protocols (structural MRI/diffusion tensor imaging/resting-state functional magnetic resonance imaging (fMRI)/positron emission tomography (PET)); (2) pre-/post-intervention longitudinal design. Risk of bias was assessed via the Newcastle-Ottawa Scale.

KEY FINDINGS

  1. Structural alterations: 7.2% mean gray matter reduction in prefrontal cortex (Cohen's d = 0.81). White matter integrity decline (FA reduction β = -0.33, < 0.001) across 12 major tracts. 2. Functional connectivity: Resting-state hyperactivity in mesolimbic pathways (fALFF + 23%, p-FDR < 0.05). Impaired fronto-striatal connectivity (r = -0.58 with BMI, 95% CI [-0.67, -0.49]). 3. Interventional reversibility: Bariatric surgery restored prefrontal activation (Δ = +18% vs. controls, = 0.002). Neurostimulation (transcranial direct current stimulation (tDCS) enhanced cognitive control (post-treatment β = 0.42, = 0.009).

CONCLUSION

  1. Obesity induces multidomain neural reorganization beyond traditional reward circuits. 2. Neuroimaging biomarkers (e.g., striatal PET-dopamine binding potential) predict intervention outcomes (AUC = 0.79). 3. Precision neuromodulation requires tripartite integration of structural guidance, functional monitoring, and molecular profiling. Findings highlight neuroimaging's pivotal role in developing stage-specific therapeutic strategies.
摘要

目的

肥胖的代谢后果已有充分记录;然而,其神经生物学基础仍不清楚。本系统评价通过先进的神经影像学综合肥胖诱导的跨结构、功能和分子领域神经可塑性的证据,填补了这一关键空白。

方法

根据PRISMA指南,我们在2015 - 2024年期间在PubMed/科学网进行了系统检索,使用医学主题词:(“肥胖”[主要主题词])AND(“神经影像学”[医学主题词]或“磁共振成像”[医学主题词])。共有104项研究符合纳入标准。纳入标准要求如下:(1)多模态成像方案(结构MRI/扩散张量成像/静息态功能磁共振成像(fMRI)/正电子发射断层扫描(PET));(2)干预前/后的纵向设计。通过纽卡斯尔-渥太华量表评估偏倚风险。

主要发现

  1. 结构改变:前额叶皮质平均灰质减少7.2%(科恩d值 = 0.81)。12条主要神经束的白质完整性下降(FA降低β = -0.33,< 0.001)。2. 功能连接:中脑边缘通路静息态活动亢进(fALFF增加23%,p-FDR < 0.05)。额纹状体连接受损(与BMI的r = -0.58,95%可信区间[-0.67, -0.49])。3. 干预可逆性:减肥手术恢复了前额叶激活(与对照组相比Δ = +18%, = 0.002)。神经刺激(经颅直流电刺激(tDCS))增强了认知控制(治疗后β = 0.42, = 0.009)。

结论

  1. 肥胖诱导了超越传统奖赏回路的多领域神经重组。2. 神经影像学生物标志物(如纹状体PET - 多巴胺结合潜能)可预测干预结果(AUC = 0.79)。3. 精准神经调节需要结构引导、功能监测和分子剖析的三方整合。研究结果突出了神经影像学在制定阶段特异性治疗策略中的关键作用。
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d9b/12109827/48bbae8b4ef0/brainsci-15-00446-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d9b/12109827/9aee6e43bd4b/brainsci-15-00446-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d9b/12109827/48bbae8b4ef0/brainsci-15-00446-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d9b/12109827/9aee6e43bd4b/brainsci-15-00446-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d9b/12109827/48bbae8b4ef0/brainsci-15-00446-g002.jpg

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The role of macrophage and adipocyte mitochondrial dysfunction in the pathogenesis of obesity.巨噬细胞和脂肪细胞线粒体功能障碍在肥胖发病机制中的作用。
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