更新于：2024-05-01

CACNA2D1

电压门控性钙通道α2/δ亚基-1

更新于：2024-05-01

基本信息

别名

CACNA2、CACNA2D1、CACNL2A

+ [11]

简介

The alpha-2/delta subunit of voltage-dependent calcium channels regulates calcium current density and activation/inactivation kinetics of the calcium channel (PubMed:35293990). Plays an important role in excitation-contraction coupling (By similarity).

关联

项与 CACNA2D1 相关的药物

Mirogabalin Besilate

苯磺酸米诺巴林

靶点

CACNA2D1 x CACNA2D2

作用机制

CACNA2D1阻滞剂 [+1]

在研机构

Daiichi Sankyo Co., Ltd.

原研机构

Daiichi Sankyo Co., Ltd.

在研适应症

神经痛 [+1]

非在研适应症

慢性肾病 [+3]

最高研发阶段批准上市

首次获批国家/地区

日本

首次获批日期2019-01-08

Gabapentin Enacarbil

加巴喷丁酯

靶点

CACNA2D1 x CACNA2D2

作用机制

CACNA2D1阻滞剂 [+1]

在研机构

Azurity Pharmaceuticals, Inc. [+2]

原研机构

XenoPort, Inc.

在研适应症

疱疹后神经痛 [+1]

非在研适应症

糖尿病性神经病变 [+2]

最高研发阶段批准上市

首次获批国家/地区

美国

首次获批日期2011-04-06

Pregabalin

普瑞巴林

靶点

CACNA2D1 x CACNA2D2

作用机制

CACNA2D1阻滞剂 [+1]

在研机构

Eisai Co., Ltd. [+14]

原研机构

The Upjohn Co.

在研适应症

纤维肌痛 [+9]

非在研适应症

乳腺癌 [+17]

最高研发阶段批准上市

首次获批国家/地区

欧盟 [+3]

首次获批日期2004-07-05

1,765

项与 CACNA2D1 相关的临床试验

ISRCTN12054536 / Recruiting临床3期IIT

Managing chronic myalgia temporomandibular disorder (M-TMD): a pragmatic phase III definitive three-arm parallel-group, co-primary outcome, individually randomised open-label controlled superiority trial comparing the clinical and cost-effectiveness and safety of Botulinum toxin type A, Lidocaine, and Amitriptyline/Gabapentin, with internal pilot and cost-effectiveness analysis (MiTiGate)

开始日期2024-06-01

申办/合作机构

The Newcastle upon Tyne Hospitals NHS Foundation Trust

NCT06383702 / Not yet recruiting临床3期

A Multicenter, Randomized, Double-Blind, Placebo-Controlled, Parallel-Controlled, Phase 3 Trial to Evaluate the Efficacy and Safety of Pregabalin Sustained-Release Tablets for the Treatment of Neuropathic Pain Associated With Diabetic Peripheral Neuropathy

This study is designed to evaluate the efficacy and safety of pregabalin extended-release tablets in the treatment of neuropathic pain associated with diabetic peripheral neuropathy. Pregabalin has been approved in more than 130 countries for neuropathic pain associated with diabetic peripheral neuropathy, postherpetic neuralgia, and neuralgia associated with spinal cord injury. Pregabalin extended-release tablets were administered once daily, as a single dose after dinner. Compared with pregabalin capsule formulation, it reduces the frequency of medication and improves patient compliance.

开始日期2024-05-15

申办/合作机构

石药集团欧意药业有限公司

NCT06367998 / Not yet recruiting临床4期IIT

The Effect of Pregabalin on Shoulder Pain of Patients With Myofascial Pain Syndrome and Central Sensitization Who Undergo Arthroscopic Rotator Cuff Repair

This study aims to investigate the effects of Pregabalin intake on shoulder pain management in patients with central sensitization undergoing arthroscopic rotator cuff repair. Although Pregabalin is known to be effective in controlling pain after shoulder arthroscopy, research on its efficacy in pain management for patients with central sensitization is scarce. Utilizing a list that identifies central sensitization, this study will explore whether Pregabalin can reduce postoperative pain in these patients and potentially improve joint mobility, emotional, and physical functioning. A prospective randomized study is planned, with inclusion criteria set for patients aged between 19 and 70 who have undergone arthroscopic rotator cuff repair.
The study will compare clinical outcomes up to one year postoperatively between two groups of 38 patients each. The case group will receive standard postoperative medications (NSAIDs) plus Pregabalin oral intake from the day before surgery to six weeks postoperatively, while the control group will receive only the standard postoperative medications without Pregabalin.

开始日期2024-05-01

申办/合作机构

The Catholic University of Korea Seoul St. Marys Hospital

[+1]

100 项与 CACNA2D1 相关的临床结果

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100 项与 CACNA2D1 相关的转化医学

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0 项与 CACNA2D1 相关的专利（医药）

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187

项与 CACNA2D1 相关的文献（医药）

2024-02-17·Experimental eye research

Influence of the calcium voltage-gated channel auxiliary subunit (CACNA2D1) absence on intraocular pressure in mice.

Article

作者: Levi Lankford ; Rupalatha Maddala ; Monica M Jablonski ; P Vasantha Rao

The etiology of elevated intraocular pressure (IOP), a major risk factor for glaucoma (optic nerve atrophy), is poorly understood despite continued efforts. Although the gene variant of CACNA2D1 (encoding α2δ1), a calcium voltage-gated channel auxiliary subunit, has been reported to be associated with primary open-angle glaucoma, and the pharmacological mitigation of α2δ1 activity by pregabalin lowers IOP, the cellular basis for α2δ1 role in the modulation of IOP remains unclear. Our recent findings reveled readily detectable levels of α2δ1 and its ligand thrombospondin in the cytoskeletome fraction of human trabecular meshwork (TM) cells. To understand the direct role of α2δ1 in the modulation of IOP, we evaluated α2δ1 null mice for changes in IOP and found a moderate (∼10%) but significant decrease in IOP compared to littermate wild type control mice. Additionally, to gain cellular insights into α2δ1 antagonist (pregabalin) induced IOP changes, we assessed pregabalin's effects on human TM cell actin cytoskeletal organization and cell adhesive interactions in comparison with a Rho kinase inhibitor (Y27632), a known ocular hypotensive agent. Unlike Y27632, pregabalin did not have overt effects on cell morphology, actin cytoskeletal organization, or cell adhesion in human TM cells. These results reveal a modest but significant decrease in IOP in α2δ1 deficient mice, and this response appears to be not associated with the contractile and cell adhesive characteristics of TM cells based on the findings of pregabalin effects on isolated TM cells. Therefore, the mechanism by which pregabalin lowers IOP remains elusive.

2024-02-12·Genes

Genome-Wide Detection for Runs of Homozygosity in Baoshan Pigs Using Whole Genome Resequencing.

Article

作者: Wenjun Li ; Xudong Wu ; Decai Xiang ; Wei Zhang ; Lingxiang Wu ; Xintong Meng ; Jinlong Huo ; Zongjun Yin ; Guowen Fu ; Guiying Zhao

Baoshan pigs (BS) are a local breed in Yunnan Province that may face inbreeding owing to its limited population size. To accurately evaluate the inbreeding level of the BS pig population, we used whole-genome resequencing to identify runs of homozygosity (ROH) regions in BS pigs, calculated the inbreeding coefficient based on pedigree and ROH, and screened candidate genes with important economic traits from ROH islands. A total of 22,633,391 SNPS were obtained from the whole genome of BS pigs, and 201 ROHs were detected from 532,450 SNPS after quality control. The number of medium-length ROH (1-5 Mb) was the highest (98.43%), the number of long ROH (>5 Mb) was the lowest (1.57%), and the inbreeding of BS pigs mainly occurred in distant generations. The inbreeding coefficient F_ROH, calculated based on ROH, was 0.018 ± 0.016, and the F_PED, calculated based on the pedigree, was 0.027 ± 0.028, which were positively correlated. Forty ROH islands were identified, containing 507 genes and 891 QTLs. Several genes were associated with growth and development (IGFALS, PTN, DLX5, DKK1, WNT2), meat quality traits (MC3R, ACSM3, ECI1, CD36, ROCK1, CACNA2D1), and reproductive traits (NPW, TSHR, BMP7). This study provides a reference for the protection and utilization of BS pigs.

2023-12-12·The Journal of neuroscience : the official journal of the Society for Neuroscience

Constitutive KCC2 cell- and synapse-specifically regulates NMDA receptor activity in the spinal cord.

Article

作者: Yuying Huang 黄玉莹 ; Hong Chen 陈红 ; Jian-Ying Shao 邵建英 ; Jing-Jing Zhou 周京京 ; Shao-Rui Chen 陈少瑞 ; Hui-Lin Pan 潘惠麟

K⁺-Cl^- cotransporter-2 (KCC2) critically controls neuronal chloride homeostasis and maintains normal synaptic inhibition by GABA and glycine. Nerve injury diminishes synaptic inhibition in the spinal cord via KCC2 impairment. However, how KCC2 regulates nociceptive input to spinal excitatory and inhibitory neurons remains elusive. Here, we show that basal GABA reversal potentials were significantly more depolarized in vesicular GABA transporter (VGAT)-expressing inhibitory neurons than in vesicular glutamate transporter-2 (VGluT2)-expressing excitatory neurons in spinal cords of male and female mice. Strikingly, inhibiting KCC2 with VU0463271 increased currents elicited by puff NMDA and the NMDAR-mediated frequency of mEPSCs in VGluT2, but not in VGAT, dorsal horn neurons. Notably, VU0463271 had no effect on EPSCs monosynaptically evoked from the dorsal root in VGluT2 neurons. Furthermore, VU0463271 augmented α2δ-1-NMDAR interactions and their protein levels in spinal cord synaptosomes. In Cacna2d1 KO mice, VU0463271 had no effect on puff NMDA currents or the mEPSC frequency in dorsal horn neurons. Disrupting α2δ-1-NMDAR interactions with α2δ-1 C-terminus mimicking peptide diminished VU0463271-induced potentiation in the mEPSC frequency and puff NMDA currents in VGluT2 neurons. Additionally, intrathecal injection of VU0463271 reduced mechanical and thermal thresholds in wild-type mice, but not in Cacna2d1 KO mice. VU0463271-induced pain hypersensitivity in mice was abrogated by co-treatment with the NMDAR antagonist, pregabalin (an α2δ-1 inhibitory ligand), or α2δ-1 C-terminus mimicking peptide. Our findings suggest that KCC2 preferentially controls presynaptic and postsynaptic NMDAR activity in excitatory dorsal horn neurons. KCC2 impairment preferentially potentiates nociceptive transmission between spinal excitatory interneurons via α2δ-1-bound NMDARs.Significance Statement Impaired function of potassium-chloride cotransporter-2 (KCC2), a key regulator of neuronal inhibition, in the spinal cord plays a major role in neuropathic pain. This study unveils that KCC2 controls spinal nociceptive synaptic strength via NMDA receptors in a cell type- and synapse type-specific manner. KCC2 inhibition preferentially augments presynaptic and postsynaptic NMDA receptor activity in spinal excitatory interneurons via α2δ-1 (previously known as a calcium channel subunit). Importantly, spinal KCC2 impairment triggers pain hypersensitivity through α2δ-1-coupled NMDA receptors. These findings pinpoint the cell and molecular substrates for the reciprocal relationship between spinal synaptic inhibition and excitation in chronic neuropathic pain. Targeting both KCC2 and α2δ-1-NMDA receptor complexes could be an effective strategy in managing neuropathic pain conditions.

项与 CACNA2D1 相关的新闻（医药）

2023-12-30

·今日头条

多吃还是少吃？10文聚焦食欲调控的奥秘

12月30日的《热心肠日报》，我们解读了 10 篇文献，关注：食欲调控，进食行为，昼夜节律，胃饥饿素，高脂饮食，暴饮暴食，医疗器械，进食障碍。 Nature：为什么吃着吃着就饱了？ Nature——[64.8] ① 当营养物质被注入胃中时，PRLH神经元通过内脏反馈表现出持续的激活，而在食物咀嚼过程中，这些持续的反应显著减少；② 相反，PRLH神经元转变为一种阶段性活动模式，这种模式与摄入时间锁定，并与食物的味道有关；③ 光遗传学揭示PRLH神经元控制秒时间尺度进食刺激的持续时间，即通过嗅觉信号反馈来抑制进食速度；④ GCG神经元被肠道的机械反馈激活，跟踪食物的消耗量，并出现持续数十分钟的饱腹感。【主编评语】一顿饭中停止进食是由尾部脑干中的专用神经回路控制的，但这些神经环路如何将进食过程中产生的感觉信号转化为行为的动态控制还需要更多研究。孤束尾核（cNTS）是大脑中第一个感知和整合许多膳食相关信号的部位，但cNTS在行为过程中如何处理摄取反馈尚不清楚。Nature近期发表的文章，通过研究进食过程对PRLH（泌乳素释放激素）和GCG神经元（两种促进非厌恶性饱腹感的主要cNTS细胞类型）的影响，发现口腔和肠道提供连续的负反馈信号，分别与尾侧脑干的不同回路相连，而尾侧脑干又控制着短时间和长时间内的进食行为。（@章台柳）【原文信息】 Sequential appetite suppression by oral and visceral feedback to the brainstem 2023-11-22, doi: 10.1038/s41586-023-06758-2 Cell：想吃咸还是想吃淡？调控盐摄取的神经通路被发现 Cell——[64.5] ① 钠离子耗竭小鼠可摄入高浓度盐水，而口渴或自由饮水小鼠则不能，通过激活pre-LC脑区神经元可促进其饮用低/高浓度盐水；② 在不影响纯水或低浓度盐水摄入下，光激活SFO-Ptger3神经元可增加小鼠对厌恶性高浓度盐溶液摄入；③ 损毁SFO-Ptger3神经元不影响钠离子耗竭激活pre-LC脑区神经元，表明前脑和后脑神经环路独立调控盐欲和盐耐受；④ 外周注射PGE2可激活SFO-Ptger3神经元，促进小鼠摄入高盐溶液，敲除Ptger3可阻断PGE2诱发的高盐耐受性。【主编评语】在钠饱和条件下，动物对低浓度钠表现出适度偏好性，对高浓度钠表现出强烈的厌恶。然而，钠耗竭的动物会大量摄入令人厌恶的高浓度盐，这种内在状态相关的钠摄入转变的神经环路机制未知。近日，加州理工学院研究人员在Cell发表最新研究，发现前脑和后脑不同的神经群以内部特定状态的方式调节盐摄入正向价值和负向价值：pre-LC脑区兴奋性神经元驱动盐欲，而SFO-Ptger3神经元驱动厌恶性盐耐受，值得关注。（@九卿臣）【原文信息】 Parallel neural pathways control sodium consumption and taste valence 2023-11-20, doi: 10.1016/j.cell.2023.10.020 Nature子刊：AgRP神经元编码昼夜节律喂养时间 Nature Neuroscience——[25] ① 小鼠神经元动力学测量和定时光遗传学激活相结合，发现AgRP神经元每日活动与现有的稳态调节模型并不完全一致；② AgRP神经元活动不是充当“剥夺计数器”，而是通过完整的视交叉上核和光同步过程遵循昼夜节律休息活动周期；③ 通过限制时间的食物获取或定期AgRP神经元刺激施加新的喂养模式，可重新同步AgRP神经元日常活动节律，并通过需要DMH PDYN神经元的过程驱动类似预期的行为。【主编评语】食物摄入按照可预测的日常模式并同步代谢节律，表达AgRP神经元可获取生理能量状态并引发进食，但目前关于这些神经元在日常时间尺度上的调节知之甚少。近日，发表在Nature Neuroscience上的这篇文章，发现AgRP神经元编码昼夜节律喂养时间，可将过去进食经历的时间信息与当前代谢需求相结合以预测昼夜节律进食时间。（@圆圈儿）【原文信息】 AgRP Neurons encode circadian feeding time 2023-11-13, doi: 10.1038/s41593-023-01482-6 Cell子刊：海马体中的胃饥饿素信号如何影响进食行为？ Neuron——[16.2] ① 研究腹侧海马在小鼠不同饥饿状态的进食行为中的作用；② 腹侧海马神经元在食物研究过程中活跃；③ 当动物研究食物时，投射到伏隔核的独特神经元亚群（vS-NAc 神经元）活动增加，并抑制进食的开始；④ 外周ghrelin水平增加，并通过突触后抑制的ghrelin受体依赖性增加，降低进食预期阶段的vS-NAc活性并促进进食的开始；⑤ 发现一个对ghrelin敏感的海马回路，可根据内部状态决定进食。【主编评语】饥饿是一种内部状态，不仅可激发进食，还可作为对预期进食相关行为进行高阶控制的线索，腹侧海马体对于区分不同环境下的最佳行为至关重要，但饥饿等内部环境如何影响海马体回路尚不清楚。近日，发表在Neuron上的这篇文章，发现通过海马体中的胃饥饿素信号对进食行为进行内部状态依赖性控制。（@圆圈儿）【原文信息】 InteRNAl-state-dependent control of feeding behavior via hippocampal ghrelin signaling 2023-11-16, doi: 10.1016/j.neuron.2023.10.016 浙大Science子刊：高脂饮食让抑制食欲的脑细胞“罢工”？ Science Advances——[13.6] ① 激活小鼠腹侧导水管灰质（vlPAG）GABA能神经元可拯救高脂饮食诱导的肥胖症，与小突触后膜电流（mIPSCs）恢复增强、能量消耗增加及腹股沟白色脂肪组织棕化有关；② 体内钙成像证实，vlPAG GABA能神经元对DIO小鼠有抑制作用，会降低内在兴奋性；③ 利用单核RNA测序监测小鼠中央导水管GABA能神经元基因表达规律，CACNA2D1在肥胖鼠中表达水平显著降低；④ 在DIO小鼠vlPAG GABA能神经元中过表达CACNA2D1可恢复增强的mIPSCs和钙响应，逆转肥胖症。【主编评语】先前有研究表明通过改变饮食结构以及生活习惯可以进行体重控制，但这类人群体重往往在5年内发生反弹。这可能与高热量食物不仅影响体重与代谢，也对中枢神经系统造成了难以逆转的改变。近日，浙江大学脑科学与脑医学学院汪浩及团队在Science Advances发表最新研究，发现中央导水管灰质区的“抑食”神经元会参与调控机体能量平衡，帮助维持体重稳态。但长期高卡食物的摄入会让这群“抑食”神经元罢工，使得动物在遇到高脂食物时欲罢不能，恶性循环的摄入过多食物，进一步探究发现CACNA2D1可能是治疗顽固性肥胖的潜在靶点，值得关注。（@九卿臣）【原文信息】 Neural adaption in midbrain GABAergic cells contributes to high-fat diet–induced obesity 2023-11-01, doi: 10.1126/sciadv.adh2884 Science子刊：未定带区多巴胺能神经元可调控饥饿状态下摄食动机行为 Science Advances——[13.6] ① 通过病毒损毁小鼠VTA脑区多巴胺能神经元，不影响其自由摄食状态下每天进食总量，而损毁ZI脑区多巴胺能神经元会显著抑制自由摄食状态下进食行为，引起体重下降；② 通过慢性激活ZI脑区多巴胺能神经元可促进小鼠通过压杆实验获得食物奖赏；③ 光激活ZI-PVT环路可促进小鼠的摄食行为，激活ZI-PAG环路几乎不影响摄食行为；④ 在24小时未进食状态下，小鼠未定带多巴神经元在靠近食物时兴奋性瞬时增强，在摄入食物过程期间神经元活性被显著抑制。【主编评语】先前研究表明敲除多巴胺后可引起严重的饥饿状态，但激活腹侧被盖区（VTA）或其下游伏隔核脑区仅仅增加小鼠进食次数，并不增加食物总消耗量。除了VTA以外，下丘脑和未定带区（ZI）也表达多巴胺能神经元。近日，佛罗里达州立大学章小兵及团队在Science Advances发表最新研究，通过动物实验，发现未定带区域一群特异性多巴胺神经元会参与饥饿状态下觅食行为动力的编码。该机制揭示了大脑如何调节摄食行为来控制进食的频率，以帮助维持机体的能量平衡，值得关注。（@九卿臣）【原文信息】 Zona incerta dopamine neurons encode motivational vigor in food seeking 2023-11-17, doi: 10.1126/sciadv.adi5326 Nature子刊：压力一大就暴食，一类神经元要负责 Nature Communications——[16.6] ① 捕食者气味（PSS）刺激暴露24小时后，小鼠的高脂饲料（HFD）食物摄入量有所增加；② 下丘脑外侧（LH）脑啡肽原（Penk）神经元由抑制性和兴奋性细胞亚群组成，直接从大脑区域接收信息，调节情绪有关反应；③ PSS小鼠的LH Penk神经元对HFD消耗表现出敏感性；④ PSS诱导的适应不良行为依赖于LH内源性脑啡肽；⑤ PSS小鼠血清皮质醇含量上升，外源皮质醇增加LH Penk神经元对HFD的反应；⑥ 抑制LH中糖皮质激素受体可逆转PSS引起的适应不良行为。【主编评语】压力大时，人们的饮食习惯很容易发生巨大的改变，有些借酒消愁，有些食欲下降，而另外一些则可能正相反、喜欢大量进食，特别是高糖高脂食物。这种压力下的饥饿及暴饮暴食，显然是心理需求而非身体饥饿的实际需求；其发生的具体机制尚不清楚。Nature Communications最新研究文章表明下丘脑外侧脑啡肽原神经元是影响的神经元适应的组成部分，是负面威胁情绪下诱发暴饮暴食的关键。（@RZN）【原文信息】 Lateral hypothalamic proenkephalin neurons drive threat-induced overeating associated with a negative emotional state 2023-10-28, doi: 10.1038/s41467-023-42623-6 Science子刊：新型电子胶囊控制食欲或可减肥 Science Advances——[13.6] ① 设计出一种可吞咽振动生物电子刺激器（VIBES）胶囊，当其到达胃部时，胃液会溶解覆盖胶囊的凝胶状膜；② VIBES可在胃里振动，激活胃部拉伸感受器，刺激迷走神经向大脑发送信号；③ 胶囊振动期间，即使动物已经禁食也会刺激饱腹感激素释放（胃饥饿素和胰高血糖素等下降），且不会增加血糖水平；④ 当机器胶囊被激活约20分钟后，再给动物提供食物，其平均食物摄入量比未激活机器胶囊时减少40%，在使用机器胶囊治疗期间，动物体重增加也更慢。【主编评语】当吃一顿大餐，胃部会向大脑发送信号，产生饱腹感进而停止进食。近日，麻省理工学院、哈佛医学院和哈佛大学研究人员在Science Advances发表最新研究，开发出一种可以在胃内振动的可摄入胶囊，这些振动会激活相同的拉伸感受器，这些感受器会在胃膨胀时感知到，从而产生一种虚幻的饱腹感。此外，在进食前20分钟服用胶囊，还使动物的食物摄入量减少约40%，值得关注。（@九卿臣）【原文信息】 A vibrating ingestible bioelectronic stimulator modulates gastric stretch receptors for illusory satiety 2023-12-22, doi: 10.1126/sciadv.adj3003 国内团队：闷热环境下为啥没食欲？肠道菌群来解答 EBioMedicine——[11.1] ① 暴露于高温高湿环境（DH）的小鼠体重增加较慢，食物摄入量较低；② 较对照小鼠，DH小鼠肠道菌群多样性改变，菌群属水平上拟普雷沃菌属、另枝杆菌属和毛螺菌科NK4A136群属富集；③ DH小鼠的粪菌导致小鼠体重增长缓慢、食物摄入量降低和肠道菌群变化；④ 采用随机森林法验证即使离开高温高湿环境后，只要肠道菌群结构保持不变，仍然可以观察到食欲抑制现象；⑤ 孟德尔随机化分析揭示毛螺菌科NK4A136群属与食欲和食欲相关激素具有显著相关性。【主编评语】食物对于维持人类和动物的重要活动至关重要。食欲控制障碍会导致各种代谢紊乱。肠道菌群组成的改变会影响食欲和能量代谢。虽然在高温高湿环境中观察到肠道菌群的变化，但高温高湿环境下肠道菌群与食欲之间的关系仍不清楚。广州中医药大学骆欢欢、陈颂及团队在EBioMedicine发表最近研究工作，揭示高温高湿环境下形成的肠道菌群具有抑制食欲以及相关激素水平的功能，这一研究为基于肠道菌群开发调节人类的食欲和代谢健康的新策略提供思路。（@RZN）【原文信息】 Gut microbiota associated with appetite suppression in high-temperature and high-humidity environments 2023-12-15, doi: 10.1016/j.ebiom.2023.104918 肠道菌群是进食障碍的罪魁祸首吗？（观点） Trends in Molecular Medicine——[13.6] ① 肠道微生物群可参与体重调节，并通过肠-脑轴影响大脑功能；② 此外，肠道微生物群可能会影响饮食失调（EDs）的发展，因为EDs患者存在与体重相关的担忧和症状；③ 如果未来的研究能够建立肠道微生物群与EDs的因果关系，肠道微生物群可能会成为治疗EDs的靶标；④ 值得提醒的是，考虑到研究力度、研究对象和所研究的ED表型，我们应该谨慎解释微生物的研究结果，合理解读肠道微生物与ED的关系。【主编评语】进食障碍（eating disorders, EDs）主要指以反常的摄食行为和心理紊乱为特征，伴有显著体质量改变和/或生理功能紊乱的一组综合征。ED可分为神经性厌食（AN）、神经性贪食（BN）和暴食症（BED）3大类。近期发表于Trends in Molecular Medicine的一篇专题论文讨论了肠道菌群与进食障碍的关联和研究进展。（@注册营养师陈彬林）【原文信息】 Eating disorders: are gut microbiota to blame? 2023-11-30, doi: 10.1016/j.molmed.2023.11.007 感谢本期日报的创作者：章台柳，九卿臣，圆圈儿，RZN，注册营养师陈彬林点击阅读过去10天的日报： 12-29 | 22页《自然·综述》讲透自闭症与胃肠道的关系 12-28 | 65分综述详解：母亲菌群如何影响孩子免疫发育？ 12-27 | Cell子刊揭秘：肠道衰老，源头在哪？ 12-26 | 《自然·综述》年度回顾：炎症性肠病疗法的新进展 12-25 | 口腔健康莫忽视！12页综述解析牙周炎与癌症的复杂关系 12-24 | 发酵食品如何促进胃肠健康？65分综述一文读懂 12-23 | 肠脑轴前沿：10文一览肠道与脑健康的紧密关系 12-22 | 《自然·综述》领衔，10文聚焦微生态干预 12-21 | 今日Nature：线粒体如何影响肠道脂代谢？ 12-20 | Nature重磅：从微生物暗物质中挖掘40万个新基因家族