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アイテム
Pathophysiological Commonality Between Irritable Bowel Syndrome and Metabolic Syndrome: Role of Corticotropin-releasing Factor-Toll-like Receptor 4-Proinflammatory Cytokine Signaling
https://asahikawa-med.repo.nii.ac.jp/records/2000472
https://asahikawa-med.repo.nii.ac.jp/records/2000472549689bd-4154-479f-ba17-ab9873cc33d3
| 名前 / ファイル | ライセンス | アクション |
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35189599.pdf (2.2 MB)
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| Item type | 学術雑誌論文 / Journal Article_02(1) | |||||||||||||||||
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| 公開日 | 2022-04-11 | |||||||||||||||||
| タイトル | ||||||||||||||||||
| タイトル | Pathophysiological Commonality Between Irritable Bowel Syndrome and Metabolic Syndrome: Role of Corticotropin-releasing Factor-Toll-like Receptor 4-Proinflammatory Cytokine Signaling | |||||||||||||||||
| 言語 | en | |||||||||||||||||
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| 言語 | eng | |||||||||||||||||
| キーワード | ||||||||||||||||||
| 主題Scheme | Other | |||||||||||||||||
| キーワード | Gut barrier | |||||||||||||||||
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| 主題Scheme | Other | |||||||||||||||||
| キーワード | Irritable bowel syndrome | |||||||||||||||||
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| 主題Scheme | Other | |||||||||||||||||
| キーワード | Metabolic syndrome | |||||||||||||||||
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| 主題Scheme | Other | |||||||||||||||||
| キーワード | Microbiota | |||||||||||||||||
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| 主題Scheme | Other | |||||||||||||||||
| キーワード | Toll-like receptor 4 | |||||||||||||||||
| 資源タイプ | ||||||||||||||||||
| 資源タイプ | journal article | |||||||||||||||||
| アクセス権 | ||||||||||||||||||
| アクセス権 | open access | |||||||||||||||||
| アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||||||||||||||
| 著者 |
野津, 司
× 野津, 司
× 奥村, 利勝
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| bibliographic_information |
en : Journal of neurogastroenterology and motility 巻 28, 号 2, p. 173-184, 発行日 2022-04-01 |
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| 収録物識別子タイプ | PISSN | |||||||||||||||||
| 収録物識別子 | 2093-0879 | |||||||||||||||||
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| 関連タイプ | isIdenticalTo | |||||||||||||||||
| 識別子タイプ | DOI | |||||||||||||||||
| 関連識別子 | https://doi.org/10.5056/jnm21002 | |||||||||||||||||
| item_1716186501932 | ||||||||||||||||||
| 識別子タイプ | PMID | |||||||||||||||||
| 関連識別子 | 35189599 | |||||||||||||||||
| item_5_description_33 | ||||||||||||||||||
| 内容記述タイプ | Abstract | |||||||||||||||||
| 内容記述 | Irritable bowel syndrome (IBS) displays chronic abdominal pain with altered defecation. Most of the patients develop visceral hypersensitivity possibly resulting from impaired gut barrier and altered gut microbiota. We previously demonstrated that colonic hyperpermeability with visceral hypersensitivity in animal IBS models, which is mediated via corticotropin-releasing factor (CRF)-Toll-like receptor 4 (TLR4)-proinflammatory cytokine signaling. CRF impairs gut barrier via TLR4. Leaky gut induces bacterial translocation resulting in dysbiosis, and increases lipopolysaccharide (LPS). Activation of TLR4 by LPS increases the production of proinflammatory cytokines, which activate visceral sensory neurons to induce visceral hypersensitivity. LPS also activates CRF receptors to further increase gut permeability. Metabolic syndrome (MS) is a cluster of cardiovascular risk factors, including insulin resistance, obesity, dyslipidemia, and hypertension, and recently several researchers suggested the possibility that impaired gut barrier and dysbiosis with low-grade systemic inflammation are involved in MS. Moreover, TLR4-proinflammatory cytokine contributes to the development of insulin resistance and obesity. Thus, the existence of pathophysiological commonality between IBS and MS is expected. This review discusses the potential mechanisms of IBS and MS with reference to gut barrier and microbiota, and explores the possibility of existence of a pathophysiological link between these diseases with a focus on CRF, TLR4, and proinflammatory cytokine signaling. We also review epidemiological data supporting this possibility, and discuss the potential of therapeutic application of the drugs used for MS to IBS treatment. This notion may pave the way for exploring novel therapeutic approaches for these disorders. | |||||||||||||||||
| 言語 | en | |||||||||||||||||
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| 出版タイプ | VoR | |||||||||||||||||
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| en | ||||||||||||||||||
| This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. | ||||||||||||||||||
