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Effects of Thiamine, Pyridoxine and Biotin on Blood Glucose Concentration and Renal Function Parameters of Alloxan-Induced Diabetic Rats

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Abstract

The aim of this study was to investigate the effects of thiamine, pyridoxine and biotin on the concentrations of blood glucose, serum electrolytes and renal functions of alloxan-induced diabetic rats. A total of twenty seven (27) adult male albino rats of Wistar strain weighing between 160-200 g were used for the study.

Twenty four (24) of the animals were rendered diabetic by a single and freshly prepared alloxan monohydrate dissolved in 0.9% ice cold normal saline solution and injected intraperitoneally at a dose of 100 mg/kg body weight.

Forty eight (48) hours after confirmation of experimental diabetes, the rats were randomly divided into nine (9) experimental groups of three (3) rats each.

Group 1 served as the normal control while Group 2 served as the diabetic control (diabetic untreated). In group 3 (standard control), metformin was used as a reference standard drug at a dose of 100 mg/kg body weight.

Group 4 (diabetic rats treated with 25 mg/kg body weight of thiamine), Group 5 (diabetic rats treated with 25 mg/kg body weight of pyridoxine), Group 6 (diabetic rats treated with 0.5 mg/kg body weight of biotin).

Introduction

Diabetes mellitus, commonly referred to as diabetes, is a metabolic disorder characterized by high blood sugar (glucose) levels over a prolonged period of time and results from defects in insulin secretion, or its action, or both (Kitabchi et al., 2009).

Normally, blood glucose levels are tightly controlled by insulin, a hormone produced by the beta cells of the pancreas.

Insulin is a water soluble hormone whose receptor is a tyrosine kinase (Rang et al., 2012). It functions primarily to lower blood glucose level by providing a mechanism for the uptake and utilization of glucose.

When the blood glucose elevates (for example after a carbohydrate rich meal), insulin is secreted from the pancreas to normalize the blood glucose level.

The inability of the pancreas to produce sufficient insulin or the cells of the body to respond to the insulin produced results in a state of hyperglycaemia and subsequently causes diabetes (David and Dolores, 2011).

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