Delphinidin 3‐rutinoside‐rich blackcurrant extract ameliorates glucose tolerance by increasing the release of glucagon‐like peptide‐1 secretion. Issue 4 (7th April 2017)

• Record Type: Journal Article
• Authors: Tani, Tsubasa; Nishikawa, Sho; Kato, Masaki; Tsuda, Takanori
• Is Part Of: Food science & nutrition. Volume 5:Issue 4(2017)
• Page Start: 929
• Page End: 933
• Publication Date: 2017-04-07
• Subjects: Anthocyanin -- blackcurrant extract -- delphinidin 3‐rutinoside -- diabetes -- glucagon‐like peptide‐1; Food industry and trade -- Periodicals; Food -- Periodicals; Nutrition -- Periodicals; 664
• DOI: 10.1002/fsn3.478
• Languages: English
• ISSNs: 2048-7177

Abstract

Abstract: Glucagon‐like peptide‐1 (GLP‐1) is an incretin that is secreted from enteroendocrine L‐cells. Dietary factor‐stimulation of endogenous GLP‐1 is a promising strategy for increasing the action of GLP‐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 GLP‐1 secretion in GLUTag cells (enteroendocrine L cell line). Blackcurrants are berries that contain high levels of anthocyanins, particularly D3R. Pre‐administered blackcurrant extract (BCE) 5 mg/kg body weight (1 mg D3R/kg) significantly ameliorated glucose tolerance after intraperitoneal glucose injection in rats by stimulating the secretion of GLP‐1 and subsequently inducing insulin secretion. D3R did not break down significantly in the gastrointestinal tract for at least 45−60 min after BCE was administered, suggesting that BCE‐induced GLP‐1 secretion is mainly mediated by D3R and not its degradation products. These findings demonstrate the novel biological function of D3R‐rich BCE as a GLP‐1 secretagogue. An increase in endogenous GLP‐1 secretion induced by BCE may help to reduce the dosages of diabetic medicines and prevent diabetes. Abstract : BCE (5 mg/kg, i.e. 1 mg D3R/kg) significantly reduces blood glucose concentration via stimulation of GLP‐1 secretion and the subsequent secretion of insulin.