Abstract

We have previously reported that Amadori compounds exert anti-diabetic effects by lowering sucrose-induced hyperglycemia in normal Sprague-Dawley rats. In the present study we extended our recent findings to evaluate whether α-glucosidase inhibitor arginyl-fructose (AF) lowers blood glucose level in diabetic db/db mice, a genetic model for type 2 diabetes. The db/db mice were randomly assigned to high-carbohydrate diets (66.1% corn starch) with and without AF (4% in the diet) for 6 weeks. Changes in body weight, blood glucose level, and food intake were measured daily for 42 days. Dietary supplementation of AF resulted in a significant decrease of blood glucose level (p < 0.001) and body weight (p < 0.001). The level of HbA1c, a better indicator of plasma glucose concentration over prolonged periods of time, was also significantly decreased for 6-week period (p < 0.001). Dietary treatment of acarbose® (0.04% in diet), a positive control, also significantly alleviated the level of blood glucose, HbA1c, and body weight. These results indicate that AF Maillard reaction product improves postprandial hyperglycemia by suppressing glucose absorption as well as decreasing HbA1c level.

Highlights

  • Non-insulin dependent diabetes mellitus (NIDDM, type 2 diabetes) is a common disorder of glucose and fat metabolism that affects approximately 171 million people worldwide, generating immense health care costs [1]

  • The effect of arginyl-fructose (AF) administration was evaluated in db/db mouse model for 42 days and compared to the effect of acarbose

  • Our observations suggest that AF supplementation in db/db mice along with high starch diet results to fasting blood glucose level, HbA1c, and total weight reductions to a similar level as acarbose, α-glucosidase inhibitor on the market (Figure 1, Table 1)

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Summary

Introduction

Non-insulin dependent diabetes mellitus (NIDDM, type 2 diabetes) is a common disorder of glucose and fat metabolism that affects approximately 171 million people worldwide, generating immense health care costs [1]. Hyperglycemia is a condition characterized by a rapid rise in blood glucose levels, which is due, primarily, to increased hydrolysis of starch by pancreatic α-amylase and α-glucosidases, leading to enhanced absorption of glucose in the small intestine. One of the therapeutic approaches for decreasing postprandial hyperglycemia is to retard absorption of glucose by the inhibition of carbohydrate hydrolyzing enzymes, mainly α-amylase and α-glucosidase, in the digestive organs [4]. Inhibition of these enzymes can significantly decrease the postprandial hyperglycemia after a mixed carbohydrate diet and can be a key strategy in the control of diabetes mellitus [5]

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