Quercetin Dampens Postprandial Hyperglycemia in Type 2 Diabetic Patients Challenged with Carbohydrates Load

Hussain S A,Aziz T A,Mahwi T O,Ahmedz A

doi:10.5923/j.diabetes.20120103.01

Hussain S A, Aziz T A + Show 2 more

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https://doi.org/10.5923/j.diabetes.20120103.01

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Abstract

Postprandial hyperglycemia is a major risk factor for diabetic co mp licat ions leading to disabilities and mortality in diabetics. Quercetin, a flavonoid, has been tried in trad itional med icine for treat ing many disorders including diabetes. The present study was designed to evaluate the potential of quercetin to damp postprandial blood glucose level after maltose and glucose loading in patients with type 2 diabetes mellitus (DM). In a rando mized, b linded crossover study, single oral dose (400mg ) of quercetin or placebo formula was ad min istered to the patients 30 min before loading with either maltose (2g/kg) or g lucose (100g), blood samp les are taken at different intervals for measurement of plas ma g lucose. The results clearly showed amelio rated postprandial hyperglycemia due to the use of quercetin, it significantly dampened the postprandial hyperglycemia only after maltose loading compared to placebo; no effect reported for quercetin after glucose loading. In conclusion, quercetin effectively suppresses postprandial hyperglycemia in patients with type 2 DM loaded with maltose, which may be attributed to α-glucosidase inhibition.

Highlights

Type 2 d iabetes is characterized by t wo main features: peripheral insulin resistance and beta-cell dysfunction
The area under the curve (AUC) for postprandial hyperglycemia, during 3 hrs after challenge with either glucose or maltose load, clearly indicated that quercetin significantly dampen postprandial hyperglycemia only after maltose challenge, while no such effect reported after administration of glucose
The data indicated that quercetin can decrease postprandial g lucose level after disaccharides loading, wh ich may be main ly attributed to inhibit ion of α-g lucosidase as one of the expected mechanis ms for the reduction of plasma glucose; this effect subsequently lead to suppression of postprandial hyperglycemia

Summary

Introduction

Type 2 d iabetes is characterized by t wo main features: peripheral insulin resistance and beta-cell dysfunction. Both hereditary and environ mental factors, such as obesity and prolonged hyperglycemia, may trigger or exaggerate hu man type 2 diabetes. Hyperglycemia causes both beta-cell damage and peripheral insulin resistance via mu ltip le mechanis ms, collectively referred to as glucotoxicity[1]. In M ODY-2 diabetes, functional defects in glucokinase genes restrict hepatic glucose uptake, bringing about prolongation of postprandial hyperglycemia[3], and eventually result in beta-cell overload. Oxidative stress, which is the result of either the overproduction of free

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