Maeda Shiro

写真a

Title

Professor

Researcher Number(JSPS Kakenhi)

50314159

Current Affiliation Organization 【 display / non-display

  • Duty   University of the Ryukyus   Graduate School of Medicine   Professor  

External Career 【 display / non-display

  • 2013.04
    -
    2016.03

    RIKEN Center for Integrative Medical Sciences  

  • 2014.08
     
     

    Graduate School of Medicine, University of the Ryukyus  

  • 2014.08
     
     

    University of the Ryukyus, Graduate School of Medicine, Professor  

Affiliated academic organizations 【 display / non-display

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    American Society of Nephrology 

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    American Diabetes Association 

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    European Association for the Study of Diabetes 

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    Japanese Society of Laboratory Medicine 

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    Japan Society of Clinical Chemistry 

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Research Interests 【 display / non-display

  • Diabetic Nephropathy

  • Diabetes Mellitus

  • Okinawa Bio-Information Bank

  • Human Genetics

  • Genome-wide association study

Research Areas 【 display / non-display

  • Life Science / Genetics

Published Papers 【 display / non-display

  • Profile of gut microbiota and serum metabolites associated with metabolic syndrome in a remote island most afflicted by obesity in Japan.

    Uema T, Millman JF, Okamoto S, Nakamura T, Yamashiro K, Uehara M, Honma KI, Miyazato M, Ashikari A, Saito S, Maeda S, Imamura M, Ishida H, Matsushita M, Nakamura K, Masuzaki H

    Scientific reports ( Scientific Reports )  12 ( 1 ) 17292   2022.10 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

  • Obesity and Voiding Parameters in a Community-Based Population of Okinawa, Japan: Kumejima Digital Health Project (KDHP).

    Ashikari A, Miyazato M, Nakamura K, Yamashiro K, Nakamura T, Uema T, Uehara M, Masuzaki H, Saito S, Maeda S, Ishida H, Matsushita M

    Metabolites ( Metabolites )  12 ( 5 )   2022.05 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

  • Multi-ancestry genetic study of type 2 diabetes highlights the power of diverse populations for discovery and translation.

    Mahajan A, Spracklen CN, Zhang W, Ng MCY, Petty LE, Kitajima H, Yu GZ, Rüeger S, Speidel L, Kim YJ, Horikoshi M, Mercader JM, Taliun D, Moon S, Kwak SH, Robertson NR, Rayner NW, Loh M, Kim BJ, Chiou J, Miguel-Escalada I, Della Briotta Parolo P, Lin K, Bragg F, Preuss MH, Takeuchi F, Nano J, Guo X, Lamri A, Nakatochi M, Scott RA, Lee JJ, Huerta-Chagoya A, Graff M, Chai JF, Parra EJ, Yao J, Bielak LF, Tabara Y, Hai Y, Steinthorsdottir V, Cook JP, Kals M, Grarup N, Schmidt EM, Pan I, Sofer T, Wuttke M, Sarnowski C, Gieger C, Nousome D, Trompet S, Long J, Sun M, Tong L, Chen WM, Ahmad M, Noordam R, Lim VJY, Tam CHT, Joo YY, Chen CH, Raffield LM, Lecoeur C, Prins BP, Nicolas A, Yanek LR, Chen G, Jensen RA, Tajuddin S, Kabagambe EK, An P, Xiang AH, Choi HS, Cade BE, Tan J, Flanagan J, Abaitua F, Adair LS, Adeyemo A, Aguilar-Salinas CA, Akiyama M, Anand SS, Bertoni A, Bian Z, Bork-Jensen J, Brandslund I, Brody JA, Brummett CM, Buchanan TA, Canouil M, Chan JCN, Chang LC, Chee ML, Chen J, Chen SH, Chen YT, Chen Z, Chuang LM, Cushman M, Das SK, de Silva HJ, Dedoussis G, Dimitrov L, Doumatey AP, Du S, Duan Q, Eckardt KU, Emery LS, Evans DS, Evans MK, Fischer K, Floyd JS, Ford I, Fornage M, Franco OH, Frayling TM, Freedman BI, Fuchsberger C, Genter P, Gerstein HC, Giedraitis V, González-Villalpando C, González-Villalpando ME, Goodarzi MO, Gordon-Larsen P, Gorkin D, Gross M, Guo Y, Hackinger S, Han S, Hattersley AT, Herder C, Howard AG, Hsueh W, Huang M, Huang W, Hung YJ, Hwang MY, Hwu CM, Ichihara S, Ikram MA, Ingelsson M, Islam MT, Isono M, Jang HM, Jasmine F, Jiang G, Jonas JB, Jørgensen ME, Jørgensen T, Kamatani Y, Kandeel FR, Kasturiratne A, Katsuya T, Kaur V, Kawaguchi T, Keaton JM, Kho AN, Khor CC, Kibriya MG, Kim DH, Kohara K, Kriebel J, Kronenberg F, Kuusisto J, Läll K, Lange LA, Lee MS, Lee NR, Leong A, Li L, Li Y, Li-Gao R, Ligthart S, Lindgren CM, Linneberg A, Liu CT, Liu J, Locke AE, Louie T, Luan J, Luk AO, Luo X, Lv J, Lyssenko V, Mamakou V, Mani KR, Meitinger T, Metspalu A, Morris AD, Nadkarni GN, Nadler JL, Nalls MA, Nayak U, Nongmaithem SS, Ntalla I, Okada Y, Orozco L, Patel SR, Pereira MA, Peters A, Pirie FJ, Porneala B, Prasad G, Preissl S, Rasmussen-Torvik LJ, Reiner AP, Roden M, Rohde R, Roll K, Sabanayagam C, Sander M, Sandow K, Sattar N, Schönherr S, Schurmann C, Shahriar M, Shi J, Shin DM, Shriner D, Smith JA, So WY, Stančáková A, Stilp AM, Strauch K, Suzuki K, Takahashi A, Taylor KD, Thorand B, Thorleifsson G, Thorsteinsdottir U, Tomlinson B, Torres JM, Tsai FJ, Tuomilehto J, Tusie-Luna T, Udler MS, Valladares-Salgado A, van Dam RM, van Klinken JB, Varma R, Vujkovic M, Wacher-Rodarte N, Wheeler E, Whitsel EA, Wickremasinghe AR, van Dijk KW, Witte DR, Yajnik CS, Yamamoto K, Yamauchi T, Yengo L, Yoon K, Yu C, Yuan JM, Yusuf S, Zhang L, Zheng W, FinnGen., eMERGE Consortium., Raffel LJ, Igase M, Ipp E, Redline S, Cho YS, Lind L, Province MA, Hanis CL, Peyser PA, Ingelsson E, Zonderman AB, Psaty BM, Wang YX, Rotimi CN, Becker DM, Matsuda F, Liu Y, Zeggini E, Yokota M, Rich SS, Kooperberg C, Pankow JS, Engert JC, Chen YI, Froguel P, Wilson JG, Sheu WHH, Kardia SLR, Wu JY, Hayes MG, Ma RCW, Wong TY, Groop L, Mook-Kanamori DO, Chandak GR, Collins FS, Bharadwaj D, Paré G, Sale MM, Ahsan H, Motala AA, Shu XO, Park KS, Jukema JW, Cruz M, McKean-Cowdin R, Grallert H, Cheng CY, Bottinger EP, Dehghan A, Tai ES, Dupuis J, Kato N, Laakso M, Köttgen A, Koh WP, Palmer CNA, Liu S, Abecasis G, Kooner JS, Loos RJF, North KE, Haiman CA, Florez JC, Saleheen D, Hansen T, Pedersen O, Mägi R, Langenberg C, Wareham NJ, Maeda S, Kadowaki T, Lee J, Millwood IY, Walters RG, Stefansson K, Myers SR, Ferrer J, Gaulton KJ, Meigs JB, Mohlke KL, Gloyn AL, Bowden DW, Below JE, Chambers JC, Sim X, Boehnke M, Rotter JI, McCarthy MI, Morris AP

    Nature genetics ( Nature Genetics )  54 ( 5 ) 560 - 572   2022.05 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

  • Impact of anti-diabetic sodium-glucose cotransporter 2 inhibitors on tumor growth of intractable hematological malignancy in humans.

    Nakachi S, Okamoto S, Tamaki K, Nomura I, Tomihama M, Nishi Y, Fukushima T, Tanaka Y, Morishima S, Imamura M, Maeda S, Tsutsui M, Matsushita M, Masuzaki H

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie ( Biomedicine and Pharmacotherapy )  149   112864   2022.05 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

  • Effect of a mobile digital intervention to enhance physical activity in individuals with metabolic disorders on voiding patterns measured by 24-h voided volume monitoring system: Kumejima Digital Health Project (KDHP).

    Miyazato M, Ashikari A, Nakamura K, Nakamura T, Yamashiro K, Uema T, Uehara M, Masuzaki H, Saito S, Maeda S, Ishida H, Matsushita M

    International urology and nephrology ( International Urology and Nephrology )  53 ( 8 ) 1497 - 1505   2021.08 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

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Grant-in-Aid for Scientific Research 【 display / non-display

  • Grant-in-Aid for Scientific Research(C)

    Project Year: 2021.04  -  2024.03 

    Direct: 3,000,000 (YEN)  Overheads: 3,900,000 (YEN)  Total: 900,000 (YEN)

  • Grant-in-Aid for Scientific Research(C)

    Project Year: 2020.04  -  2023.03 

    Direct: 3,300,000 (YEN)  Overheads: 4,290,000 (YEN)  Total: 990,000 (YEN)

  • Identification of novel therapeutic target for type 2 diabetes through genome-based drug discovery

    Grant-in-Aid for Scientific Research(C)

    Project Year: 2017.04  -  2020.03 

    Investigator(s): Imamura Minako 

    Direct: 3,500,000 (YEN)  Overheads: 4,550,000 (YEN)  Total: 1,050,000 (YEN)

     View Summary

    Genome-wide association studies (GWAS) have identified more than 200 genetic loci associated with susceptibility for type 2 diabetes (T2D). We have previously proposed several new potential pharmacological targets for T2D treatments using systematic bioinformatics approach integrating the findings of GWAS for T2D, and biological or pharmacological information from various databases. KIF11 is one of the potential therapeutic targets identified by the in silico pipeline. We have demonstrated that administration of KIF11 inhibitor ameliorated impaired glucose tolerance on db/db mice through increasing the insulin sensitivity and suppressing hepatic glucose production. The results suggest that our GWAS-based drug discovery platform is useful to identify novel drug targets for the treatment of common diseases, such as T2D.

  • Comprehensive analysis of autophagy in the pathogenesis of diabetes and its complications

    Grant-in-Aid for Scientific Research(B)

    Project Year: 2014.04  -  2018.03 

    Investigator(s): Maegawa Hiroshi, KUME Shinji, MAEDA Shiro, YAMAHARA Mako, TAGAWA Atsuko, YOSHIBAYASHI Mamoru 

    Direct: 12,700,000 (YEN)  Overheads: 16,510,000 (YEN)  Total: 3,810,000 (YEN)

     View Summary

    Autophagy is an intracellular catabolic process that can maintain cellular homeostasis during several stress conditions such as starvation and mitochondrial oxidative stress. Growing evidences have shown that altered autophagy activity is associated with the pathogenesis of a variety of diseases. The present study revealed that mammalian autophagy is essential for maintaining energy homeostasis via enhancing ketogenesis during starvation, and that diabetes-related dysregulation of autophagy is involved in the pathogenesis of diabetic vascular complications, such as diabetic nephropathy. These observation suggest that autophagy activation should shed a light on therapy for diabetic complications and contribute to health promotion in diabetic patients.

  • Functional analysis of GWAS-derived type 2 diabetes susceptibility genes

    Grant-in-Aid for Scientific Research(C)

    Project Year: 2014.04  -  2017.03 

    Investigator(s): IMAMURA Minako 

    Direct: 3,800,000 (YEN)  Overheads: 4,940,000 (YEN)  Total: 1,140,000 (YEN)

     View Summary

    We have performed a fine-mapping within the C2CD4A-C2CD4B locus to identify causal variants for type 2 diabetes susceptibility. The most significant association was observed in intergenic region which indicates the causal variant may affect the expression of either C2CD4A or C2CD4B. We also found that these genes dominantly expressed in human pancreas and mouse pancreatic beta cell line. Motivated by the results of fine mapping and expression analysis, we have generated beta-cell specific transgenic mice for C2cd4a and C2cd4b respectively to evaluate the role of these genes in vivo.

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