The analysis of fagopyritols from tartary buckwheat and their anti-diabetic effects in KK-Ay type 2 diabetic mice and HepG2 cells. (November 2018)

• Record Type: Journal Article
• Authors: Wu, Weijing; Wang, Lijuan; Qiu, Ju; Li, Zaigui
• Is Part Of: Journal of functional foods. Volume 50(2018)
• Page Start: 137
• Page End: 146
• Publication Date: 2018-11
• Subjects: Fagopyritols -- Tartary buckwheat -- Glucose and lipid metabolism -- Insulin sensitivity -- Insulin signaling; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2018.09.032
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: Highlights: The content of fagopyritols was more than 10 folds of DCI in tartary buckwheat. The fagopyritols and DCI improved glucose and lipid metabolism in KK-A y mice. The fagopyritols and DCI enhanced the glucose consumption in HepG2 cells. The fagopyritols and DCI may play the role through phosphorylation of PI3K/AKT. Abstract: The studies of fagopyritols in tartary buckwheat and their anti-diabetic effects are limited. The fagopyritol B1 was the major fagopyritol in tartary buckwheat. The content of fagopyritols was 11-fold of free D-chiro-inositol (DCI) in tartary buckwheat. In KK-A y mice, administration of fagopyritol B1 for 6-week was more effective in suppressing progressive rise of blood glucose, improving impaired glucose tolerance, and increasing insulin sensitivity than DCI and fagopyritol A1. Besides, both of fagopyritols and DCI improved the lipid homeostasis. Fagopyritols increased the expression of insulin receptor and PI3K in liver and skeletal muscle, as the same as DCI. According to the in vitro study, fagopyritols and DCI increased glucose consumption in both normal and insulin resistant HepG2 cells. In addition, fagopyritols and DCI upregulated phosphorylation of PI3K and AKT. In summary, these findings suggested that fagopyritols and DCI have potential anti-diabetic effects via activation of the insulin dependent pathway of PI3K/AKT.