藤田 浩樹 (フジタ ヒロキ)

FUJITA Hiroki

写真a

所属

大学院医学系研究科(医学専攻等)  医学専攻  社会環境医学系  先端医学研究推進講座

研究キーワード 【 表示 / 非表示

  • インクレチンの膵外作用

  • 糖尿病性腎症と酸化ストレス

  • 糖尿病性腎症モデルマウスの開発

  • 高齢者糖尿病におけるフレイル・サルコペニア・認知症

  • GLP-1の腎保護作用

出身大学 【 表示 / 非表示

  •  
    -
    1995年03月

    新潟大学   医学部   卒業

出身大学院 【 表示 / 非表示

  •  
    -
    2001年03月

    秋田大学  医学研究科  博士課程  修了

取得学位 【 表示 / 非表示

  • 秋田大学 -  医学博士

職務経歴(学内) 【 表示 / 非表示

  • 2025年03月
    -
    継続中

    秋田大学   大学院医学系研究科(医学専攻等)   医学専攻   社会環境医学系   先端医学研究推進講座   特任教授  

  • 2018年04月
    -
    2025年02月

    秋田大学   大学院医学系研究科(医学専攻等)   医学専攻   病態制御医学系   准教授  

  • 2007年10月
    -
    2018年03月

    秋田大学   附属病院   老年科   講師  

研究分野 【 表示 / 非表示

  • ライフサイエンス / 内科学一般

  • ライフサイエンス / 腎臓内科学

  • ライフサイエンス / 代謝、内分泌学

 

研究等業績 【 表示 / 非表示

    ◆原著論文【 表示 / 非表示

  • GLP-1 receptor signaling restores aquaporin 4 subcellular polarization in reactive astrocytes and promotes amyloid β clearance in a mouse model of Alzheimer's disease

    Sasaki K.

    Biochemical and Biophysical Research Communications ( Biochemical and Biophysical Research Communications )  741   151016 - 151016   2024年12月  [査読有り]

    研究論文(学術雑誌)   国内共著

    The physiological actions of a gut hormone, glucagon-like peptide-1 (GLP-1), in Alzheimer's disease (AD) brain remain poorly understood, although GLP-1 receptor (GLP-1R) expression in this organ has been shown in several experimental studies. Therefore, we explored whether the GLP-1R signaling promotes the clearance of amyloid β (Aβ) (1-42) which is a core pathological hallmark of AD, focusing on the water channel protein aquaporin 4 (AQP4) localized to astrocyte endfeet perivascular membranes in intact brain. First, we confirmed that Glp1r mRNA is predominantly expressed at perivascular site of astrocytes in normal mouse cerebral cortex through in situ hybridization analysis. Next, we observed that 20-week subcutaneous administration of a GLP-1R agonist (GLP-1RA) liraglutide significantly reduced Aβ (1-42) accumulation in the cerebral cortex and improved spatial working memory in an AD mouse model, AppNL-G-F/NL-G-F mice. Furthermore, our current data revealed that the 4-week liraglutide treatment relocalized subcellular AQP4 in morphologically injured reactive astrocytes of AppNL-G-F/NL-G-F mice to the cell surface perivascular site through PKA-mediated AQP4 phosphorylation. Such translocation of phosphorylated AQP4 to astrocyte cell surface following incubation with liraglutide was observed also in the present in vitro study using the cell line in which AQP4 cDNA was introduced into immortalized human astrocyte. These results suggest that enhanced intracerebral GLP-1R signaling following peripheral administration of GLP-1RA restores AQP4 subcellular polarization in reactive astrocytes and would promote Aβ excretion possibly through increasing AQP4-mediated intracerebral water flux in the brain in AD.

    DOI PubMed

  • Multidomain Intervention Trial for Preventing Cognitive Decline among Older Adults with Type 2 Diabetes: J-MIND-Diabetes

    Sugimoto T.

    Journal of Prevention of Alzheimer's Disease ( Journal of Prevention of Alzheimer's Disease )  11 ( 6 ) 1604 - 1614   2024年12月  [査読有り]

    研究論文(学術雑誌)   国内共著

    DOI

  • Recurrent nocturnal hypoglycemic hemiplegia: a case report and review of the literature

    Toyama H.

    Endocrine Journal ( Endocrine Journal )  71 ( 4 ) 409 - 416   2024年  [査読有り]

    研究論文(学術雑誌)   国内共著

    A 67-year-old man with type 1 diabetes, Cronkhite-Canada syndrome, and membranous nephropathy who received insulin therapy was admitted to our hospital with right hemiplegia and dysarthria. Brain magnetic resonance imaging revealed a lesion with a high diffusion-weighted imaging signal and low apparent diffusion coefficient signal in the posterior limb of the left internal capsule. He was hypoglycemic with a blood glucose level of 56 mg/dL (3.1 mmol/L). Following glucose administration, the patient's symptoms resolved within several hours. The patient experienced similar transient hypoglycemic hemiplegia at midnight, three times within 10 days. In a literature review of 170 cases of hypoglycemic hemiplegia, 26 cases of recurrent hemiplegia were investigated. Recurrent hypoglycemic hemiplegia occurs more frequently on the right side than on the left side, and most recurrences occur within approximately a week, almost exclusively at midnight and in the early morning. We speculate that hypoglycemia-associated autonomic failure may be involved in the nocturnal recurrence of episodes. In our patient, depleted endogenous insulin secretion and lipodystrophy at the injection site, may have acted as additional factors, leading to severe hypoglycemia despite the absence of apparent autonomic neuropathy. Clinically, it is important to recognize hypoglycemia as a cause of hemiplegia to avoid unnecessary intervention and to maintain an appropriate blood glucose level at midnight and early in the morning to prevent recurrent hypoglycemic hemiplegia.

    DOI PubMed CiNii Research

  • Gastric inhibitory polypeptide receptor antagonism suppresses intramuscular adipose tissue accumulation and ameliorates sarcopenia

    Takahashi Y.

    Journal of Cachexia, Sarcopenia and Muscle ( Journal of Cachexia, Sarcopenia and Muscle )  14 ( 6 ) 2703 - 2718   2023年12月  [査読有り]

    研究論文(学術雑誌)   国内共著

    BACKGROUND: Intramuscular adipose tissue (IMAT) formation derived from muscle fibro-adipogenic progenitors (FAPs) has been recognized as a pathological feature of sarcopenia. This study aimed to explore whether genetic and pharmacological gastric inhibitory polypeptide (GIP) receptor antagonism suppresses IMAT accumulation and ameliorates sarcopenia in mice. METHODS: Whole body composition, grip strength, skeletal muscle weight, tibialis anterior (TA) muscle fibre cross-sectional area (CSA) and TA muscle IMAT area were measured in young and aged male C57BL/6 strain GIP receptor (Gipr)-knockout (Gipr-/- ) and wild-type (Gipr+/+ ) mice. FAPs isolated from lower limb muscles of 12-week-old Gipr+/+ mice were cultured with GIP, and their differentiation into mature adipocytes was examined. Furthermore, TA muscle IMAT area and fibre CSA were measured in untreated Gipr-/- mice and GIP receptor antagonist-treated Gipr+/+ mice after glycerol injection into the TA muscles. RESULTS: Body composition analysis revealed that 104-week-old Gipr-/- mice had a greater proportion of lean tissue mass (73.7 ± 1.2% vs. 66.5 ± 2.7%, P < 0.05 vs. 104-week-old Gipr+/+ mice) and less adipose tissue mass (13.1 ± 1.3% vs. 19.4 ± 2.6%, P < 0.05 vs. 104-week-old Gipr+/+ mice). Eighty-four-week-old Gipr-/- mice exhibited increases in grip strength (P < 0.05), weights of TA (P < 0.05), soleus (P < 0.01), gastrocnemius (P < 0.05) and quadriceps femoris (P < 0.01) muscles, and average TA muscle fibre CSA (P < 0.05) along with a reduction in TA muscle IMAT area assessed by the number of perilipin-positive cells (P < 0.0001) compared with 84-week-old Gipr+/+ mice. Oil Red O staining analysis revealed 1.6- and 1.7-fold increased adipogenesis in muscle FAPs cultured with 10 and 100 nM of GIP (P < 0.01 and P < 0.001 vs. 0 nM of GIP, respectively). Furthermore, both untreated Gipr-/- mice and GIP receptor antagonist-treated Gipr+/+ mice for 14 days after glycerol injection into the TA muscles at 12 weeks of age showed reduced TA muscle IMAT area (1.39 ± 0.38% and 2.65 ± 0.36% vs. 6.54 ± 1.30%, P < 0.001 and P < 0.01 vs. untreated Gipr+/+ mice, respectively) and increased average TA muscle fibre CSA (P < 0.01 and P < 0.05 vs. untreated Gipr+/+ mice, respectively). CONCLUSIONS: GIP promotes the differentiation of muscle FAPs into adipocytes and its receptor antagonism suppresses IMAT accumulation and promotes muscle regeneration. Pharmacological GIP receptor antagonism may serve as a novel therapeutic approach for sarcopenia.

    DOI PubMed

  • Efficacy and Safety of 6-Month High Dietary Protein Intake in Hospitalized Adults Aged 75 or Older at Nutritional Risk: An Exploratory, Randomized, Controlled Study

    Shota Moyama, Yuichiro Yamada, Noboru Makabe, Hiroki Fujita, Atsushi Araki, Atsushi Suzuki, Yusuke Seino, Kenichiro Shide, Kyoko Kimura, Kenta Murotani, Hiroto Honda, Mariko Kobayashi, Satoshi Fujita, Koichiro Yasuda, Akira Kuroe, Katsushi Tsukiyama, Yutaka Seino, Daisuke Yabe

    Nutrients     2023年04月  [査読有り]

    研究論文(学術雑誌)   国内共著

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  • 食事療法と認知機能障害

    藤田浩樹

    Progress in Medicine ( ライフ・サイエンス )  43 ( 12 ) 1109 - 1114   2023年12月

    総説・解説(商業誌)   単著

  • 糖尿病性腎症におけるインクレチンの腎保護作用

    藤田浩樹

    BIO Clinica ( 北陸館 )  38 ( 5 ) 450 - 453   2023年05月

    総説・解説(商業誌)   単著

  • GLP-1の腎保護効果

    藤田浩樹

    Precision Medicine ( 北陸館 )  5 ( 8 ) 763 - 766   2022年08月

    総説・解説(商業誌)   単著

  • 糖尿病性腎症における血管平滑筋GLP-1 受容体シグナルの役割

    藤田浩樹

    Medical Science Digest ( ニューサイエンス社 )  48 ( 2 ) 99 - 101   2022年02月

    総説・解説(商業誌)   単著

  • 高齢者糖尿病診療Update―「高齢者糖尿病治療ガイド2021」を読み解く― 4. 高齢者糖尿病の食事療法

    藤田浩樹

    糖尿病プラクティス ( 医歯薬出版 )  39 ( 1 ) 33 - 38   2022年01月

    総説・解説(商業誌)   単著

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  • 術前にチルゼパチドを使用し食行動質問票の改善と減量が得られた高度肥満症の1例

    照井 幹司, 高橋 和之, 小木田 彩香, 加藤 俊祐, 安藤 清香, 奈良 光彦, 佐藤 雄大, 森井 宰, 藤田 浩樹, 脇 裕典

    糖尿病 ( (一社)日本糖尿病学会 )  67 ( 5 ) 227 - 227   2024年05月

  • GIPシグナルの抑制は骨格筋内脂肪の蓄積を減少させてサルコペニアの改善に寄与する

    高橋 侑也, 藤田 浩樹, 脇 裕典, 山田 祐一郎

    糖尿病 ( (一社)日本糖尿病学会 )  67 ( Suppl.1 ) S - 161   2024年04月

  • コルチゾール測定法の変更に伴う副腎不全の診断率の変化とカットオフ値の検討

    加藤俊祐, 加藤俊祐, 赤沼英, 奈良光彦, 清水辰徳, 清水辰徳, 佐藤雄大, 森井宰, 藤田浩樹, 脇裕典

    日本内分泌学会雑誌   100 ( 1 )   2024年

    J-GLOBAL

  • 脂肪組織のNFIA遺伝子メチル化の肥満と脂質制御における役割

    清水 辰徳, 大口 弥里, 青山 倫久, 加藤 俊祐, 佐藤 雄大, 森井 宰, 藤田 浩樹, 大田 秀隆, 堤 修一, 安田 和基, 藤坂 志帆, 戸邉 一之, 成田 伸太郎, 羽渕 友則, 山内 敏正, 脇 裕典

    肥満研究 ( (一社)日本肥満学会 )  29 ( 合同学術集会抄録集 ) 287 - 287   2023年11月

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  • 高齢者糖尿病診療ガイドライン2023、Ⅶ. 高齢者糖尿病の食事療法

    藤田浩樹、佐藤雄大、山田祐一郎 ( 担当: 分担執筆 )

    南江堂  2023年05月

    学術書

  • 高齢者糖尿病治療ガイド2021、5. 高齢者糖尿病の食事療法

    藤田浩樹、山田祐一郎 他、日本糖尿病学会・日本老年医学会(編) ( 担当: 分担執筆 )

    文光堂  2021年05月

    学術書

産業財産権 【 表示 / 非表示

  • サルコペニア予防及び/又は治療用医薬組成物、サルコペニア予防及び/又は治療剤、並びにサルコペニアの予防及び/又は治療方法

    特許

    特願 特願2023-069858 

    出願日: 2023年04月21日

    髙橋侑也 , 藤田浩樹 , 山田祐一郎 , 矢部大介

  • クルクミン誘導体の利用

    特許

    特願 特願2022-171661 

    出願日: 2022年10月26日

    柴田浩行、藤田浩樹、髙橋侑也、恩田浩幸、安永 新

科研費(文科省・学振)獲得実績 【 表示 / 非表示