Delphinidin 3‐rutinoside‐rich blackcurrant extract ameliorates glucose tolerance by increasing the release of glucagon‐like peptide‐1 secretion

  • Tsubasa Tani
    College of Bioscience and Biotechnology Chubu University Kasugai Aichi Japan
  • Sho Nishikawa
    College of Bioscience and Biotechnology Chubu University Kasugai Aichi Japan
  • Masaki Kato
    College of Bioscience and Biotechnology Chubu University Kasugai Aichi Japan
  • Takanori Tsuda
    College of Bioscience and Biotechnology Chubu University Kasugai Aichi Japan

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<jats:title>Abstract</jats:title><jats:p>Glucagon‐like peptide‐1 (<jats:styled-content style="fixed-case">GLP</jats:styled-content>‐1) is an incretin that is secreted from enteroendocrine L‐cells. Dietary factor‐stimulation of endogenous <jats:styled-content style="fixed-case">GLP</jats:styled-content>‐1 is a promising strategy for increasing the action of <jats:styled-content style="fixed-case">GLP</jats:styled-content>‐1. Recent studies have shown that berries rich in anthocyanins improve insulin sensitivity and reduce the risk of type 2 diabetes. Our previous study found that the anthocyanin delphinidin 3‐rutinoside (D3R) significantly increases <jats:styled-content style="fixed-case">GLP</jats:styled-content>‐1 secretion in <jats:styled-content style="fixed-case">GLUT</jats:styled-content>ag cells (enteroendocrine L cell line). Blackcurrants are berries that contain high levels of anthocyanins, particularly D3R. Pre‐administered blackcurrant extract (<jats:styled-content style="fixed-case">BCE</jats:styled-content>) 5 mg/kg body weight (1 mg D3R/kg) significantly ameliorated glucose tolerance after intraperitoneal glucose injection in rats by stimulating the secretion of <jats:styled-content style="fixed-case">GLP</jats:styled-content>‐1 and subsequently inducing insulin secretion. D3R did not break down significantly in the gastrointestinal tract for at least 45−60 min after <jats:styled-content style="fixed-case">BCE</jats:styled-content> was administered, suggesting that <jats:styled-content style="fixed-case">BCE</jats:styled-content>‐induced <jats:styled-content style="fixed-case">GLP</jats:styled-content>‐1 secretion is mainly mediated by D3R and not its degradation products. These findings demonstrate the novel biological function of D3R‐rich <jats:styled-content style="fixed-case">BCE</jats:styled-content> as a <jats:styled-content style="fixed-case">GLP</jats:styled-content>‐1 secretagogue. An increase in endogenous <jats:styled-content style="fixed-case">GLP</jats:styled-content>‐1 secretion induced by <jats:styled-content style="fixed-case">BCE</jats:styled-content> may help to reduce the dosages of diabetic medicines and prevent diabetes.</jats:p>

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