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井上 朋也大学院医学系研究科 医科学専攻研究員
研究活動情報
■ 受賞- 2026年02月 日本糖尿病・肥満動物学会, 若手研究奨励賞
- 2025年08月 日本筋学会, 若手研究奨励賞
- 2025年06月 日本内分泌学会学, 若手研究奨励賞
- 2025年04月 日本臨床分子医学会, 学術奨励賞受賞
- 2024年12月 分子糖尿病学シンポジウム, 若手研究奨励賞
- 2024年07月 日本内分泌学会, 内分泌代謝学サマーセミナー ポスター賞
- 2024年05月 日本糖尿病学会, 若手研究奨励賞
- ABSTRACT Aims/Introduction Obesity is often accompanied by skeletal muscle atrophy, which aggravates insulin resistance and metabolic dysfunction. Chronic inflammation is implicated in this process, but the molecular mediators linking obesity‐induced inflammation to muscle wasting have remained unclear. We investigated the role of the chemokine CXCL10 in skeletal muscle inflammation and atrophy induced by a high‐fat diet (HFD). Materials and Methods Male C57BL/6J mice were fed an HFD or normal diet for 2 weeks and received either neutralizing antibodies to CXCL10 or control immunoglobulin G. Muscle morphology, macrophage infiltration, and gene expression were examined by histology, immunohistochemistry, reverse transcription–quantitative polymerase chain reaction analysis, and RNA sequencing. Cultured C2C12 myotubes were also treated with recombinant CXCL10 or lipopolysaccharide (LPS), with or without antibodies to CXCL10, for assessment of direct effects on myotube atrophy. Results HFD feeding upregulated Cxcl10 expression in skeletal muscle. It also induced fiber atrophy, macrophage infiltration, and increased expression of individual inflammation‐ or proteolysis‐related genes in muscle, with these effects being attenuated by CXCL10 neutralization. Transcriptomic analysis further revealed a broad reversal of HFD‐induced changes in gene expression related to protein catabolism and myofiber structure by anti‐CXCL10 administration. Both CXCL10 and LPS reduced myotube diameter and increased expression of catabolism‐ or inflammation‐related genes in cultured C2C12 myotubes, whereas CXCL10 blockade prevented these effects of LPS. Conclusions CXCL10 mediates HFD‐induced skeletal muscle atrophy by promoting inflammation and proteolysis. CXCL10 neutralization mitigates such muscle loss and may represent a novel therapeutic strategy to preserve skeletal muscle mass under metabolic stress.Wiley, 2026年02月, Journal of Diabetes Investigation[査読有り]研究論文(学術雑誌)
- (一社)日本肥満学会, 2025年10月, 肥満研究, 31(合同学術集会抄録集) (合同学術集会抄録集), 314 - 314, 日本語肝細胞のPiezo 1活性化によるMASLD進展抑制効果の解析
- (一社)日本糖尿病学会, 2025年10月, 糖尿病, 68(10) (10), 400 - 408, 日本語[査読有り]
- (一社)日本糖尿病インフォマティクス学会, 2025年08月, 日本糖尿病インフォマティクス学会年次学術集会プログラム・抄録集, 25回, 60 - 60, 日本語不動化が腸管組織に与える影響およびメトホルミン・イメグリミンによる効果 single-cell RNA-seq解析
- (一社)日本筋学会, 2025年08月, 日本筋学会学術集会プログラム・抄録集, 11回, 66 - 66, 日本語運動による筋量増加における機械刺激感受性イオンチャネルPiezo1の機能解析
- Piezo1, a mechanosensitive ion channel that opens in response to mechanical stimuli, is widely expressed among mammalian cell types, and regulates a diverse range of physiological processes. Although evidence has suggested potential clinical benefit of Piezo1 activation for various conditions, the safety and efficacy of such activation in living animals have remained unclear. To investigate the therapeutic potential of Piezo1 activation, we here generated genetically modified mouse models in which Piezo1 is overexpressed either specifically in skeletal muscle or systemically in response to tamoxifen treatment in adult animals. Cast immobilization induced a reduction in both muscle mass and the abundance of Piezo1 mRNA in skeletal muscle of the affected limbs in control mice. Overexpression of Piezo1 in skeletal muscle prevented the immobilization-induced reduction both in soleus muscle mass and in the corresponding cross-sectional area of myofibers, suggesting the potential benefit of Piezo1 activation for prevention of immobilization-induced muscle atrophy. Furthermore, mice with systemic overexpression of Piezo1 showed no apparent abnormalities in growth or general activity. Red blood cells from these mice manifested slight resistance to hypoosmolarity-induced hemolysis, and the animals did not develop apparent hemolytic anemia. Our findings demonstrate promising efficacy and safety of Piezo1 activation in living animals and thereby highlight the therapeutic potential of targeting the Piezo1 signaling pathway.2025年05月, The Kobe journal of medical sciences, 71(1) (1), E31-E40, 英語, 国内誌[査読有り]研究論文(学術雑誌)
- (一社)日本糖尿病学会, 2025年04月, 糖尿病, 68(Suppl.) (Suppl.), S - 272, 日本語公開データベースを用いたin silico解析による運動依存性新規経路探索の試み
- 2025年, 日本内分泌学会雑誌, 101(1) (1)運動による筋量増加における機械刺激感受性イオンチャネルPiezo1の機能解析
- 2024年, 糖尿病(Web), 67(Suppl) (Suppl)機械刺激感受性イオンチャネルPiezo1を介した筋肥大機構の解明
- 2024年, 日本内分泌学会内分泌代謝学サマーセミナープログラム・講演要旨集(Web), 42nd運動における機械刺激感受性イオンチャネルPiezo1の機能の解明
- Coronavirus disease 2019 (COVID-19) is associated with endocrine disorders, but their long-term clinical course remains unclear. We here report the 15-month clinical course for an individual with multiple endocrine disorders of the pituitary gland and testis likely triggered by COVID-19. A 65-year-old man with no history of endocrinopathy was admitted for acute COVID-19 pneumonia. Although his respiratory condition improved after administration of antiviral drugs, his blood pressure dropped suddenly to a preshock level and was refractory to vasopressors. The circulating adrenocorticotropic hormone (ACTH) and cortisol concentrations were low, and secondary adrenal insufficiency was suspected. Administration of hydrocortisone rapidly ameliorated the hypotension, and the patient was discharged taking 15 mg of hydrocortisone daily. An insulin tolerance test performed 3 months later revealed impaired ACTH, cortisol, and growth hormone (GH) responses, indicative of combined hypopituitarism. The patient also manifested symptoms of hypogonadism, and a hormonal workup suggested primary hypogonadism. At 12 months after discharge, GH and ACTH responses had recovered completely and partially, respectively. After another 3 months, basal ACTH and cortisol levels had been restored to the normal range and the patient discontinued hydrocortisone replacement without exacerbation of symptoms, although his hypogonadism persisted. The patient thus developed transient GH and ACTH deficiency that lasted for more than a year as well as persistent primary hypogonadism during intensive care for COVID-19. Certain prolonged symptoms of COVID-19 might be accounted for by such hormonal disturbance.2022年11月, Endocrine journal, 69(11) (11), 1335 - 1342, 英語, 国内誌[査読有り]研究論文(学術雑誌)
- (一社)日本糖尿病学会, 2022年04月, 糖尿病, 65(Suppl.1) (Suppl.1), S - 169, 日本語免疫チェックポイント阻害薬投与後に発症した1型糖尿病様の糖尿病の特徴と膵臓MRI所見との関連についての検討
- (一社)日本糖尿病学会, 2021年05月, 糖尿病, 64(Suppl.1) (Suppl.1), I - 3, 日本語CSII療法施行中1型糖尿病患者の朝食絶食による血中ケトン体推移に関する検討
- 2024年, 糖尿病(Web), 67(Suppl) (Suppl)腸管-骨格筋相互作用による筋量制御のメカニズム
- 2024年, 糖尿病(Web), 67(Suppl) (Suppl)四肢固定中の筋肉の炎症と萎縮における筋神経腸管ネットワークの役割
- 2022年, 糖尿病(Web), 65(Suppl) (Suppl)免疫チェックポイント阻害薬投与後に発症した1型糖尿病様の糖尿病の特徴と膵臓MRI所見との関連についての検討
- (一社)日本糖尿病学会, 2021年05月, 糖尿病, 64(Suppl.1) (Suppl.1), I - 3, 日本語CSII療法施行中1型糖尿病患者の朝食絶食による血中ケトン体推移に関する検討
- 2021年, 糖尿病ケア糖尿病治療薬の使いかたと処方のポイント 2 ビグアナイド薬の処方のポイント
- 2021年, 糖尿病(Web), 64(Suppl) (Suppl)CSII療法施行中1型糖尿病患者の朝食絶食による血中ケトン体推移に関する検討
- 2020年, 糖尿病(Web), 63(7) (7)持続皮下インスリン注入療法(CSII)導入後に著明な肝腫大を認めた1型糖尿病患者の1例
- 2020年, 糖尿病(Web), 63(7) (7)2型糖尿病に合併した周期性ACTH-ADH放出症候群の1例
- 2020年, 糖尿病(Web), 63(Suppl) (Suppl)各種GLP-1受容体作動薬の腎機能に与える効果についての検討
- 2020年, 糖尿病(Web), 63(Suppl) (Suppl)各種GLP-1受容体作動薬のNASH/NAFLDに対する有用性の検討~薬剤間の差を含めて~
- 2019年, 日本内分泌学会雑誌, 95(2) (2)レボチロキシン過量内服による著明な甲状腺中毒症を繰り返した一例
- 2019年, 日本内分泌学会雑誌, 95(2) (2)抗PD-L1抗体製剤の使用後下垂体前葉機能低下症を来した肺癌の1例
- 2019年, 糖尿病(Web), 62(Suppl) (Suppl)当院における世界糖尿病デーイベント開催に向けて~企画から開催までの経過とアンケート結果より~
- 2019年, 糖尿病(Web), 62(4) (4)1型糖尿病診断前に低血糖様発作を繰り返した1例
- 2019年, 糖尿病(Web), 62(Suppl) (Suppl)SGLT2阻害薬の長期効果(特に肝機能改善効果)についての検討
- 2019年, 糖尿病(Web), 62(Suppl) (Suppl)糖尿病に合併した閉塞性動脈硬化症とそのリスク因子との関連性についての検討
- 2019年, 糖尿病(Web), 62(4) (4)ヘモクロマトーシスにより血糖コントロール悪化をきたした2型糖尿病の1例
- 2018年, 日本内分泌学会雑誌, 94(2) (2)多彩な内分泌異常を呈したヘモクロマトーシスの一例
- 2017年, 日本内分泌学会雑誌, 93(2) (2)GAD抗体高値を伴う糖尿病の経過中にアジソン病を発症した1例
■ 共同研究・競争的資金等の研究課題
