Abstract
Fagopyrum tataricum (buckwheat) is used for the treatment of type 2 diabetes mellitus in Taiwan. This study was to evaluate the antihyperglycemic and anti-insulin resistance effects of 75% ethanol extracts of buckwheat (EEB) in FL83B hepatocytes by high-glucose (33 mM) induction and in C57BL/6 mice by fructose-rich diet (FRD; 60%) induction. The active compounds of EEB (100 μg/mL; 50 mg/kg bw), quercetin (6 μg/mL; 3 mg/kg bw), and rutin (23 μg/mL; 11.5 mg/kg bw) were also employed to treat FL83B hepatocytes and animal. Results indicated that EEB, rutin, and quercetin + rutin significantly improved 2-NBDG uptake via promoting Akt phosphorylation and preventing PPARγ degradation caused by high-glucose induction for 48 h in FL83B hepatocytes. We also found that EEB could elevate hepatic antioxidant enzymes activities to attenuate insulin resistance as well as its antioxidation caused by rutin and quercetin. Finally, EEB also inhibited increases in blood glucose and insulin levels of C57BL/6 mice induced by FRD.
Highlights
Type 2 diabetes mellitus (T2DM) is a chronic disease caused by deficient insulin secretion or ineffective insulin activity, which negatively affects carbohydrate metabolism
Results suggested that 228.8 mg/g of rutin and 58.6 mg/g of quercetin were contained in ethanol extracts of buckwheat (EEB) (Figure 1)
We evaluated the effects of EEB, rutin, and quercetin on the insulin resistance pathway in FL83B hepatocytes with high-glucose-level-induced insulin resistance
Summary
Type 2 diabetes mellitus (T2DM) is a chronic disease caused by deficient insulin secretion or ineffective insulin activity, which negatively affects carbohydrate metabolism. Hepatic regulation of glucose homeostasis is the major factor controlling plasma glucose concentrations, and the induction of hepatic ER stress and oxidative stress resulting in insulin resistance has been investigated [1]. High-fructose diet upregulates hepatic expression of the sterol regulatory element binding protein-1c (SREBP-1c), a key transcription factor for hepatic expression of lipogenic enzymes, but down regulates the expression of PPARα (promoting fatty acid oxidation) [2, 3]. The study investigates the fructose-inducing effect in C57BL/6 mice and has found that fructose would promote SREBP-1c promoter activity resulting in hepatic lipogenesis [4]. Fructose is employed to induce insulin resistance, hepatic steatosis, and the metabolic syndrome [5]. Fructose is a highly lipogenic sugar that has profound metabolic effects in the liver resulting in metabolic syndrome, and fructose does not stimulate insulin secretion [6]. Fructose may activate SREBP-1c which activates genes involved in de novo lipogenesis, and triglyceride [8]
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