SATOH Tatsuya

写真a

Affiliation

School of Medicine, Department of Physiology

Job title

Associate Professor
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Research Experience 【 display / non-display 】

  • 2024.01
    -
    Now

    Sapporo Medical University   School of Medicine   Associate Professor

  • 2022.03
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    2023.12

    Sapporo Medical University   School of Medicine Medical Sciences   Assistant Professor

  • 2017.04
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    2022.03

    Sapporo Medical University   Department of Cellular Physiology and Signal Transduction   Assistant Professor

  • 2013.10
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    2016.03

    Northwestern University Feinberg Cardiovascular Research Institute   Postdoctoral Research Fellow

  • 2011.04
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    2013.03

    Sapporo Medical University School of Medicine   Department of Cellular Physiology and Signal Transduction   Assistant Professor

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Professional Memberships 【 display / non-display 】

  • 2023.04
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    Now

    日本肥満学会

  • 2022.04
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    Now

    日本内分泌学会

  • 2019
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    Now

    日本医師会

  • 2017
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    Now

    日本心不全学会

  • 2017
    -
    Now

    日本糖尿病協会

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Research Areas 【 display / non-display 】

  • Life sciences   Nephrology  

  • Life sciences   Physiology  

  • Life sciences   Cardiology  

  • Life sciences   Metabolism and endocrinology  

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Affiliation 【 display / non-display 】

  • Sapporo Medical University   Department of Cellular Physiology and Signal Transduction, School of Medicine   Associate Professor  

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Research Interests 【 display / non-display 】

  • Electrophysiology

  • Cardioprotection

  • Mitochondrial function

  • 運動・筋生理学

  • 糖尿病慢性合併症

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Papers 【 display / non-display 】

  • Deciphering metabolic dysfunction-associated steatotic liver disease: insights from predictive modeling and clustering analysis.

    Kazuma Mori, Yukinori Akiyama, Marenao Tanaka, Tatsuya Sato, Keisuke Endo, Itaru Hosaka, Nagisa Hanawa, Naoya Sakamoto, Masato Furuhashi

    Journal of gastroenterology and hepatology    2024.04  [Refereed]  [International journal]

    　View Summary

    BACKGROUND AND AIM: New nomenclature of steatotic liver disease (SLD) including metabolic dysfunction-associated SLD (MASLD), MASLD and increased alcohol intake (MetALD), and alcohol-associated liver disease (ALD) has recently been proposed. We investigated clustering analyses to decipher the complex landscape of SLD pathologies including the former nomenclature of nonalcoholic fatty liver disease (NAFLD) and metabolic dysfunction-associated fatty liver disease (MAFLD). METHODS: Japanese individuals who received annual health checkups including abdominal ultrasonography (n = 15 788, men/women: 10 250/5538, mean age: 49 years) were recruited. RESULTS: The numbers of individuals with SLD, MASLD, MetALD, ALD, NAFLD, and MAFLD were 5603 (35.5%), 4227 (26.8%), 795 (5.0%), 324 (2.1%), 3982 (25.8%), and 4946 (31.3%), respectively. Clustering analyses using t-distributed stochastic neighbor embedding and K-means to visually represent interconnections in SLDs uncovered five cluster formations. MASLD and NAFLD mainly shared three clusters including (i) low alcohol intake with relatively low-grade obesity; (ii) obesity with dyslipidemia; and (iii) dysfunction of glucose metabolism. Both MetALD and ALD displayed one distinct cluster intertwined with alcohol consumption. MAFLD widely shared all of the five clusters. In machine learning-based analyses using algorithms of random forest and extreme gradient boosting and receiver operating characteristic curve analyses, fatty liver index (FLI), calculated by body mass index, waist circumference, and levels of γ-glutamyl transferase and triglycerides, was selected as a useful feature for SLDs. CONCLUSIONS: The new nomenclature of SLDs is useful for obtaining a better understanding of liver pathologies and for providing valuable insights into predictive factors and the dynamic interplay of diseases. FLI may be a noninvasive predictive marker for detection of SLDs.

    DOI PubMed

  • Differential Effects of Benzalkonium Chloride on Human Trabecular Meshwork Cells Not Treated or Treated with Transforming Growth Factor-β2 or Dexamethasone.

    Megumi Watanabe, Tatsuya Sato, Araya Umetsu, Nami Nishikiori, Megumi Higashide, Masato Furuhashi, Hiroshi Ohguro

    Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics    2024.03  [Refereed]  [International journal]

    　View Summary

    Purpose: The objective of the present study was to evaluate the effects of low concentrations of benzalkonium chloride (BAC) (10-7%, 10-6%, or 10-5%) on healthy and glaucomatous human trabecular meshwork (HTM) cells. For this purpose, we used in vitro models replicating a healthy HTM and HTM with primary open-angle glaucoma (POAG) or steroid-induced glaucoma (SG) using two-dimensional (2D) cultures of HTM cells not treated or treated with a 5 ng/mL solution of transforming growth factor-β2 or 250 nM dexamethasone (DEX). Methods: Analyses were carried out for (1) the intercellular affinity function of 2D HTM monolayers, as determined by transepithelial electrical resistance (TEER) measurements; (2) cell viability; (3) cellular metabolism by using a Seahorse bioanalyzer; and (4) expression of extracellular matrix (ECM) molecules, an ECM modulator, and cell junction-related molecules. Results: In the absence and presence of BAC (10-7% or 10-5%), intercellular affinity function determined by TEER and cellular metabolic activities were significantly and dose dependently affected in both healthy and glaucomatous HTM cells despite the fact that there was no significant decrease in cell viabilities. However, the effects based on TEER values were significantly greater in the healthy HTM. The mRNA expression of several molecules that were tested was not substantially modulated by these concentrations of BAC. Conclusions: The findings reported herein suggest that low concentrations of BAC may have unfavorable adverse effects on cellular metabolic capacity by inducing increases in the intercellular affinity properties of the HTM, but those effects of BAC were different in healthy and glaucomatous HTM cells.

    DOI PubMed

  • Downregulation of Mitochondrial Fusion Protein Expression Affords Protection from Canonical Necroptosis in H9c2 Cardiomyoblasts

    Yuki Toda, SANG-BING ONG, Toshiyuki Yano, Atsushi Kuno, Hidemichi Kouzu, Tatsuya Sato, Wataru Ohwada, Yuki Tatekoshi, Toshifumi Ogawa, Masaki Shimizu, Masaya Tanno, Masato Furuhashi

    International Journal of Molecular Sciences    2024.03  [Refereed]

    DOI

  • Bob1 maintains T follicular helper cells for long-term humoral immunity

    Masahiro Yanagi, Ippei Ikegami, Ryuta Kamekura, Tatsuya Sato, Taiki Sato, Shiori Kamiya, Kosuke Murayama, Sumito Jitsukawa, Fumie Ito, Akira Yorozu, Miho Kihara, Takaya Abe, Hiromi Takaki, Koji Kawata, Katsunori Shigehara, Satsuki Miyajima, Hirotaka Nishikiori, Akinori Sato, Noritsugu Tohse, Ken-ichi Takano, Hirofumi Chiba, Shingo Ichimiya

    Communications Biology   7 ( 185 )  2024.02  [Refereed]

    DOI

  • Platelet-rich plasma does not accelerate the healing of damaged muscle following muscle strain.

    Hiroyori Fusagawa, Takashi Yamada, Tatsuya Sato, Yuki Ashida, Atsushi Teramoto, Hiroyuki Takashima, Azuma Naito, Nao Tokuda, Nao Yamauchi, Nobutoshi Ichise, Izaya Ogon, Toshihiko Yamashita, Noritsugu Tohse

    Journal of orthopaedic research : official publication of the Orthopaedic Research Society    2024.01  [Refereed]  [International journal]

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    Although platelet-rich plasma (PRP) has been widely used regardless of the severity of muscle strain, there have been very few basic studies in which its effects on muscle injury were examined by using models that accurately mimic the clinical muscle strain injury process. Therefore, the aim of this study was to confirm by physiological and structural analyses whether PRP purified by a general preparation method has a muscle healing effect on muscle damage caused by eccentric contraction (ECC). Male Wistar rats were subjected to muscle injury induced by ECC in bilateral plantar flexor muscles using electrical stimulation and an automatically dorsiflexing footplate. The rats were randomly assigned to three groups by type of injection: phosphate-buffered saline (PBS), leukocyte-poor PRP (LP-PRP), or leukocyte-rich PRP (LR-PRP) injection into gastrocnemius muscles three times at weekly intervals. The platelet concentrations of the LP-PRP and LR-PRP were three to five times higher than that of whole blood. The recovery process of torque strength in the plantar flexor muscle, signal changes in MRI images, and histological evaluation 3 weeks after injury showed no obvious differences among the three groups, and every muscle recovered well from the injury without marked fibrosis. The results that neither LP-PRP nor LR-PRP was found to accelerate healing of muscle injuries suggested that conventional preparation and use of PRP for simple muscle injuries caused by muscle strain should be carefully considered, and further basic research using models that accurately mimic clinical practice should be carried out to determine the optimal use of PRP.

    DOI PubMed

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Misc 【 display / non-display 】

  • ガイドニードルを用いた超音波ガイド下腎生検は手技時間を短縮する

    小松弘明, 山下智久, 長南新太, 赤澤史子, 遠藤康太, 津川舜, 宮森大輔, 木村歩, 安部功記, 高橋聖子, 後町結, 佐藤達也, 小山雅之, 田中希尚, 矢野俊之, 茂庭仁人

    日本腎臓学会誌(Web)   64 ( 3 )  2022

    J-GLOBAL

  • Sensor augmented pump使用下にリツキシマブ投与と二重濾過血漿交換を行い良好な経過を辿ったB型インスリン受容体異常症の1例

    赤澤史子, 長南新太, 佐藤達也, 神田真聡, 馬場周平, 小松弘明, 村瀬和幸, 北尾直之, 山下智久, 矢野俊之

    糖尿病(Web)   65 ( Suppl )  2022

    J-GLOBAL

  • 糖尿病合併心不全における血漿分枝鎖アミノ酸の規定因子と予後予測能の検討

    神津英至, 片野唆敏, 大堀克彦, 大堀克彦, 長岡凌平, 沼澤瞭, 小山雅之, 小山雅之, 永野伸卓, 藤戸健史, 大和田渉, 佐藤達也, 矢野俊之

    糖尿病(Web)   65 ( Suppl )  2022

    J-GLOBAL

  • AMP Deaminase in Mitochondria-Associated ER Membranes Contributes to Reduction of the Threshold for Mitochondrial Permeability Transition in Type 2 Diabetic Hearts

    Arata Osanami, Masaya Tanno, Atsushi Kuno, Hidemichi Kouzu, Toshiyuki Yano, Tatsuya Sato, Tetsuji Miura, Toshifumi Ogawa

    CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  144  2021.11

    Research paper, summary (international conference)  

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    0

  • AMPデアミナーゼによる心臓分岐鎖アミノ酸代謝の新規制御 糖尿病性心筋症の治療標的としての期待(Novel Regulation of Cardiac Branched-chain Amino Acid Metabolism through AMP Deaminase: A Possible Therapeutic Target for Diabetic Cardiomyopathy)

    Ogawa Toshifumi, Kouzu Hidemichi, Osanami Arata, Tatekoshi Yuki, Mizuno Masashi, Kuno Atsushi, Sugawara Hirohito, Fujita Yugo, Ino Shoya, Ohwada Wataru, Sato Tatsuya, Yano Toshiyuki, Moniwa Norihito, Tanno Masaya, Miura Tetsuji

    日本循環器学会学術集会抄録集 ( (一社)日本循環器学会 )  85回   OE081 - 3  2021.03

    J-GLOBAL

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Awards 【 display / non-display 】

  • 第1回日本循環器学会基礎研究フォーラム Poster Award

    2018.01   The Japanese Circulation Society   Tristetraprolin prevents iron deficiency-induced ROS production by optimizing expression of UQCRFS1.

  • 第34回ISHR日本部会 YIA優秀賞

    2017.12   International Society for Heart Research（ISHR）Japanese Section of ISHR   A novel role of tristetraprolin in regulation of reactive oxygen species production by optimizing iron containing proteins

  • 第21回日本心不全学会学術集会 基礎の部 YIA優秀賞

    2017.10   The Japanese Heart Failure Society   Tristetraprolin-mediated regulation of Rieske, a mitochondrial complex III protein, protects the heart against iron deficiency.

  • FCVB - European Society of Cardiology 2016 Moderated Poster Award

    2016.07   European Society of Cardiology   A novel role of tristetraprolin in preventing mitochondrial dysfunction in the heart against iron deficiency by optimizing expression of Rieske iron-sulfur protein

  • 第90回 日本生理学会年次学術集会 佐川喜一賞

    2013.03   The Japan Physiological Society   Characteristics of Voltage Dependent Inward Currents in the Rat Embryonic Heart Early After the Initiation of Heartbeat

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Research Projects 【 display / non-display 】

  • 腎不全サルコペニアの運動時エネルギー代謝障害の解明と神経-筋電気刺激療法の確立

    基盤研究(C)

    Project Year :

    2023.04
    -
    2026.03
     

    房川 祐頼, 佐藤 達也, 山田 崇史

    Authorship： Coinvestigator(s)

  • 低酸素誘導因子1α が胎生初期心臓原基の拍動開始および拍動維持に及ぼす影響の検討

    基盤研究(C)

    Project Year :

    2022.04
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    2025.03
     

    當瀬 規嗣, 佐藤 達也, 一瀬 信敏

  • Targeting ROS-induced ROS release in mitochondria as a therapeutic strategy for diabetes-associated heart failure.

    Grant-in-Aid for Scientific Research (C)

    Project Year :

    2022.04
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    2025.03
     

    佐藤 達也, 矢野 俊之

  • 糖尿病による骨髄由来細胞の質的変化 ～ヒト血液細胞を用いた探索的研究～

    基盤研究(C)

    Project Year :

    2022.04
    -
    2025.03
     

    山下 智久, 佐藤 達也

  • Effects of impaired response to myocardial mitochondrial iron depletion on the development of heart failure

    Grant-in-Aid for Scientific Research (C)

    Project Year :

    2019.04
    -
    2022.03
     

    SATO TATSUYA

    　View Summary

    Systemic iron deficiency exacerbates the prognosis of cardiovascular disease, but its mechanisms are unknown. In this study, we focused on the role of impaired response to iron deficiency in the myocardial mitochondria in the subtotal nephrectomized rat (SNx), which is a model of the failing heart with systemic iron deficiency. Contrary to decreased serum iron levels, the amount of heme iron in myocardial mitochondria was increased and oxidative stress was enhanced in SNx. Increased expression of ALAS2, a rate-limiting enzyme in the mitochondrial heme synthesis pathway and the increased production of reactive oxygen species by the Fenton reaction were suggested as mechanisms for the phenotypes. These findings indicate that impaired response to iron deficiency in the myocardial mitochondria in the failing hearts is associated with cellular death and cardiac dysfunction. Impaired mitochondrial iron response may be a novel therapeutic target for heart failure.

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Teaching Experience 【 display / non-display 】

  • Physiology  

    2017.04
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    Now
     

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Committee Memberships 【 display / non-display 】

  • 2024.04
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    Now

      The board of physiological education

  • 2023.04
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    2025.03

      医学系CBT実施管理委員

  • 2023.04
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    2024.03

      医学系CBT実施管理委員会機構派遣監督者専門部会 委員

  • 2019.04
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    Now

      評議員

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