A Noninvasive Metabolic Syndrome Model Using an Extremely Small Minipig, the Microminipig

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Author(s)

    • Yamazaki Takanori Miura Katsuyuki
    • Department of Pharmacology, Osaka City University Medical School, Japan |Applied Pharmacology and Therapeutics, Osaka City University Medical School, Japan
    • Yoshiyama Minoru
    • Department of Cardiovascular Medicine, Osaka City University Medical School, Japan
    • Izumi Yasukatsu
    • Department of Pharmacology, Osaka City University Medical School, Japan
    • Yamazaki Takanori
    • Department of Cardiovascular Medicine, Osaka City University Medical School, Japan
    • Kawaguchi Hiroaki
    • Laboratory of Veterinary Histopathology, Joint Faculty of Veterinary Medicine, Kagoshima University, Japan
    • Tawa Masashi
    • Department of Pharmacology, Shiga University of Medical Sciences, Japan
    • Nakamura Yasuhiro
    • Department of Cardiovascular Medicine, Osaka City University Medical School, Japan|Department of Cardiology, Izumi Municipal Hospital, Japan
    • Shiota Masayuki
    • Department of Pharmacology, Osaka City University Medical School, Japan
    • Osada-Oka Mayuko
    • Department of Pharmacology, Osaka City University Medical School, Japan |Food Hygiene and Environmental Health Division of Applied Life Science, Kyoto Prefectural University, Japan
    • Tanimoto Akihide
    • Department of Molecular and Cellular Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Japan
    • Okamura Tomio
    • Department of Pharmacology, Shiga University of Medical Sciences, Japan

Abstract

Metabolic syndrome (MetS) induces serious complications; therefore, we developed a noninvasive MetS model using an extremely small minipig, the Microminipig. For 8 weeks, Microminipigs were administrated a high-fat and high-cholesterol diet (HFCD) for atherosclerosis and <i>N</i><sup>G</sup>-nitro-<span style="font-variant: small-caps;">l</span>-arginine methyl ester (<span style="font-variant: small-caps;">l</span>-NAME) for inhibiting nitric oxide synthase. HFCD significantly increased serum low-density lipoprotein levels, <span style="font-variant: small-caps;">l</span>-NAME increased blood pressure and cardiac hypertrophy, and HFCD-induced aortal arteriosclerosis was accelerated by <span style="font-variant: small-caps;">l</span>-NAME administration. Endothelium-dependent relaxation of the coronary artery was remarkably decreased by <span style="font-variant: small-caps;">l</span>-NAME administration. This model may be useful for elucidating the mechanisms of MetS and developing new therapeutic medicines for its treatment.

Journal

  • Journal of Pharmacological Sciences

    Journal of Pharmacological Sciences 126(2), 168-171, 2014

    The Japanese Pharmacological Society

Codes

  • NII Article ID (NAID)
    130004690915
  • NII NACSIS-CAT ID (NCID)
    AA11806667
  • Text Lang
    ENG
  • ISSN
    1347-8613
  • NDL Article ID
    025861795
  • NDL Call No.
    Z53-D199
  • Data Source
    NDL  J-STAGE 
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