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Intake of soy foods regulates the development of metabolic syndrom

Research Project

Project/Area Number 25350126
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Eating habits
Research InstitutionThe University of Tokushima

Principal Investigator

SAKAI Tohru  徳島大学, 大学院医歯薬学研究部, 教授 (40274196)

Research Collaborator SHUTO Emi  
KIOKA Miku  
NAKAMOTO Mariko  
MITANI Mami  
Project Period (FY) 2013-04-01 – 2016-03-31
Project Status Completed (Fiscal Year 2015)
Budget Amount *help
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywords大豆 / アレルギー / 免疫 / 疫学 / メタボリックシンドローム / エクオール / 内臓脂肪 / 炎症 / イソフラボン / 肥満
Outline of Final Research Achievements

In this study, we examined effect of soy-related ingredients on the development of metabolic syndrome in animal model and human study. Treatment of soy isoflavone equol improved blood glucose levels following oral glucose or insulin administration in mice fed high-fat diet. Treatment equol reduced visceral fat weight. Equol tended to decrease mRNA expression of inflammatory cytokines in visceral fat.
We studied 452 Japanese individuals who completed a baseline (2009-2010) and follow-up survey (2012-2013). Abdominal circumference, systolic and diastolic blood pressure, blood glucose level, serum triglyceride and HDL-cholesterol levels were used as component of metabolic syndrome. The standard partial regression coefficient (β) for abdominal circumference of miso intake was -0.208 (p=0.016) in men under 40 years, though there is no significant association between miso intake and components of metabolic syndrome in men 40 and older.

Report

(4 results)
  • 2015 Annual Research Report   Final Research Report ( PDF )
  • 2014 Research-status Report
  • 2013 Research-status Report
  • Research Products

    (8 results)

All 2015 2014 2013

All Journal Article (7 results) (of which Int'l Joint Research: 2 results,  Peer Reviewed: 7 results,  Open Access: 3 results,  Acknowledgement Compliant: 3 results) Book (1 results)

  • [Journal Article] Dietary ribonucleic acid suppresses inflammation of adipose tissue and improves glucose intolerance that is mediated by immune cells in C57BL/6 mice fed a high-fat diet.2015

    • Author(s)
      Sakai T, Taki T, Nakamoto A, Tazaki S, Arakawa M, Nakamoto M, Tsutsumi R, Shuto E.
    • Journal Title

      J. Nutr. Sci. Vitaminol.

      Volume: 61 Pages: 73-78

    • NAID

      130005070836

    • Related Report
      2015 Annual Research Report 2014 Research-status Report
    • Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
  • [Journal Article] Vitamin A deficiency impairs induction of oral tolerance in mice.2015

    • Author(s)
      Nakamoto A, Shuto E, Tsutsumi R, Nakamoto A, Sakai T.
    • Journal Title

      J. Nutr. Sci. Vitaminol.

      Volume: 63 Pages: 143-153

    • NAID

      130005074125

    • Related Report
      2015 Annual Research Report 2014 Research-status Report
    • Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
  • [Journal Article] Treatment with buckwheat bran extract prevents the elevation of serum triglyceride levels and fatty liver in KK-Ay mice.2014

    • Author(s)
      Hosaka T., Sasaga S., Yamasaka Y., Nii Y., Edazawa K., Tsutsumi R., Shuto E., Okahisa N., Iwata S., Tomotake H., and Sakai T.
    • Journal Title

      J. Med. Invest.

      Volume: 61 Pages: 342-352

    • NAID

      130004822740

    • Related Report
      2014 Research-status Report
    • Peer Reviewed / Open Access / Acknowledgement Compliant
  • [Journal Article] Treatment with buckwheat bran extract prevents the elevation of serum triglyceride levels and fattu liver in KK-Ay mice.2014

    • Author(s)
      Hosaka T., Sasaga S., Yamasaka Y., Nii Y., Edazawa K., Tsutsumi R., Shuto E., Okahisa N., Iwata S., Tomotake H., and Sakai T.
    • Journal Title

      J. Med. Investi.

      Volume: 3

    • Related Report
      2013 Research-status Report
    • Peer Reviewed
  • [Journal Article] Lactobacillus plantarum OLL2712 regulates glucose metabolism in C57BL/6 mice fed a high-fat diet.2013

    • Author(s)
      Sakai T., Taki T., Nakamoto A., Shuto E., Tsutsumi R., Toshimitsu T., Makino S., and Ikegami S.
    • Journal Title

      J. Nutr. Sci. Vitaminol.

      Volume: 59 Pages: 144-147

    • NAID

      130003368160

    • Related Report
      2013 Research-status Report
    • Peer Reviewed
  • [Journal Article] Association between blood levels of PCDDs/PCDFs/dioxin-like PCBs and history of allergic and other diseases in the Japanese population2013

    • Author(s)
      Nakamoto M., Arisawa K., Uemura H.,Katsuura S, Takami H., Sawachika F., Yamaguchi M., Juta T., Sakai T., Toda E., Mori K., Hasegawa M., Tanto M., Shima M., Sumiyoshi Y., Morinaga K., Kodama K., Suzuki T., Nagai M., and Satoh H.
    • Journal Title

      International Archives of Occupational and Environmental Health

      Volume: 86 Pages: 849-859

    • Related Report
      2013 Research-status Report
    • Peer Reviewed
  • [Journal Article] Cysteine string protein 1 (CSP1) modulates insulin sensitivity by attenuating glucose transporter 4 (GLUT4) vesicle docking with the plasma membrane.2013

    • Author(s)
      Jambaldoei B., Terada E., Hosaka T., Kishuku Y., Tomioka Y., Iwashima K., Hirata Y., Teshigawara K., Le C.T.K., Nakagawa T., Harada N., Sakai T., Sakaue H., Matsumoto T., Funaki M., Takahashi A., and Nakaya Y.
    • Journal Title

      J. Med. Investi.

      Volume: 60 Pages: 197-204

    • NAID

      130004822683

    • Related Report
      2013 Research-status Report
    • Peer Reviewed
  • [Book] 公衆栄養学2015

    • Author(s)
      酒井徹
    • Total Pages
      25
    • Publisher
      講談社
    • Related Report
      2014 Research-status Report

URL: 

Published: 2014-07-25   Modified: 2019-07-29  

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