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Research Article| Volume 57, ISSUE 9, P1299-1306, September 2008

Miglitol suppresses the postprandial increase in interleukin 6 and enhances active glucagon-like peptide 1 secretion in viscerally obese subjects

  • Masayuki Arakawa
    Affiliations
    Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, Tokyo, Japan
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  • Chie Ebato
    Affiliations
    Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, Tokyo, Japan
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  • Tomoya Mita
    Affiliations
    Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, Tokyo, Japan
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  • Yoshio Fujitani
    Affiliations
    Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, Tokyo, Japan

    Center for Therapeutic Innovations in Diabetes, Juntendo University School of Medicine, Tokyo, Japan
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  • Tomoaki Shimizu
    Affiliations
    Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, Tokyo, Japan
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  • Hirotaka Watada
    Affiliations
    Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, Tokyo, Japan
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  • Ryuzo Kawamori
    Affiliations
    Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, Tokyo, Japan

    Center for Therapeutic Innovations in Diabetes, Juntendo University School of Medicine, Tokyo, Japan
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  • Takahisa Hirose
    Correspondence
    Corresponding author. Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunky-ku, Tokyo 113-8421, Japan. Tel.: +81 3 5802 1579; fax: +81 3 3813 5996.
    Affiliations
    Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, Tokyo, Japan

    Center for Therapeutic Innovations in Diabetes, Juntendo University School of Medicine, Tokyo, Japan
    Search for articles by this author

      Abstract

      Visceral obesity and insulin resistance are regarded as risk factors for atherosclerosis. Epidemiologic studies have demonstrated long-term anti-atherosclerotic effects with administration of α-glucosidase inhibitors. α-Glucosidase inhibitors also have been reported to enhance glucagon-like peptide 1 (GLP-1) secretion. We compared the postprandial effects of a single administration of miglitol and acarbose on glucose and lipid metabolism, on insulin requirement, on GLP-1 secretion, and on inflammatory and endothelial markers in viscerally obese subjects. Twenty-four viscerally obese subjects with relative insulin resistance participated in this study. Subjects were given a single dose of miglitol (50 mg), acarbose (100 mg), or placebo blindly and randomly before a meal in a crossover design. The meal loads after drug administration were tested 3 times within 2 weeks. We measured glucose, insulin, lipids, lipoprotein lipase, interleukin 6, intracellular adhesion molecule 1, vascular cell adhesion molecule 1, and active GLP-1 at before and various minutes after the meal. Single administration of both α-glucosidase inhibitors had several beneficial effects in improving postprandial hyperglycemia and reducing postprandial insulin requirement approximately 25% of placebo without adversely affecting lipid profiles. Although lipoprotein lipase levels within 2 hours after the meal did not show differences among miglitol, acarbose, and placebo administrations, miglitol significantly suppressed the increases in triglycerides, remnant-like particle triglycerides, and remnant-like particle cholesterol compared to acarbose and placebo in the early phase. Miglitol also significantly enhanced active GLP-1 secretion to a greater extent than acarbose (P < .01) and placebo (P < .001), and significantly suppressed the postprandial increase in interleukin 6 compared to placebo (P < .01). The results point to the potential suitability of miglitol as an anti-atherosclerotic effect in viscerally obese subjects, in preference to acarbose. Further studies are needed to elucidate the long-term effects on enhanced GLP-1 secretion and anti-atherosclerosis.
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