Abstract

Metformin is widely used for type II diabetes. Sugar replacement sweeteners such as Aspartame and Stevia, are usually consumed concomitantly with other antidiabetics by patients The aim of this work is to investigate possible effects of two types of sweeteners; stevia and aspartame on the pharmacokinetic parameters of metformin in rats. A simple, validated bio-analytical HPLC method was developed to measure metformin in rat plasma. Three groups of rats, each of eight were subjected to this study. The first group was given metformin solution 20mg/kg alone , the second group was given 20 mg/kg metformin with 4mg/kg stevia and the third group was given 20 mg/kg metformin with 10 mg/kg aspartame on fasting state. Blood samples were taken on scheduled time interval up to 6 hours and analyzed for metformin concentration. Pharmacokinetic parameters were calculated by Non-Compartmental Model and data were interpreted. The results showed that administration of these two sweeteners did not have high effect on pharmacokinetics of metformin.

Highlights

  • Metformin is a biguanide oral hypoglycemic agent which is commonly used in type II diabetes mellitus

  • Sugar replacement sweeteners such as Aspartame and Stevia, are usually consumed concomitantly with other antidiabetics by patients The aim of this work is to investigate possible effects of two types of sweeteners; stevia and aspartame on the pharmacokinetic parameters of metformin in rats

  • The results showed that administration of these two sweeteners did not have high effect on pharmacokinetics of metformin

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Summary

Introduction

Metformin is a biguanide oral hypoglycemic agent which is commonly used in type II diabetes mellitus. It was introduced after the restriction of phenformin due to less side effect especially lactic acidosis (Berbman, 1978). It was approved by FDA 1n 1994.Metformin exerts its activity by multiphase effects on GIT in lowering glucose absorption and liver by inhibition of glucose synthesis as well as increasing glucose uptake by cells without increasing the level of insulin (Hermann and Malender, 1992; Cusi and Defr, 1998).

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