Abstract

Objectives: The study aimed to determine the effect of coffee intake on AGEs formation and platelet aggregation in diabetic Wistar rats. Methods: Coffee powder samples were used to prepare a 10% beverage. Diabetes mellitus was induced in the animals by administering 2% alloxan. All animal experiments were approved by the ethics committee for animal experiments under N°. 420/2012 and 536/2013. Diabetic and non-diabetic rats were divided into 6 groups treated and untreated with coffee (7.2 mL/Kg body weight) and aminoguanidine (AGE inhibiting agent) (100 mg/Kg body weight) for 50 days. After 50 days, the animals were fasted for 12 h and anesthetized (40 mg/Kg sodium pentobarbital) intraperitoneally. Blood samples were collected from the abdominal artery puncture. Hematological parameters (red cells, hemoglobin, hematocrit and leukocyte) and glycemic and HbA1c levels were measured. AGEs quantification (spectrofluorometric method) and the platelet aggregation test (aggregation of cuvettes in a four-channel platelet aggregometer) were also conducted. The rats’ renal function was evaluated by measuring serum urea and creatinine. Results: Data showed that coffee intake had no effect on the hematological parameters. Fasting glucose and HbA1c dosage were significantly higher in diabetic animals compared to non-diabetic animals (confirmed the effectiveness of inducing and maintaining diabetic status). Results showed that coffee reduced AGE formation and platelet aggregation in our animal model, not altering the animals’ renal function. Conclusions: These results suggest beneficial effects on vasculopathy, a common complication in diabetic patients.

Highlights

  • Diabetes mellitus (DM) is a chronic metabolic disease characterized by hyperglycemia that affects 415 million people worldwide, with an estimate for the coming decades of 642 million new cases[1,2]

  • Complications resulting from chronic hyperglycemia during DM are caused by oxidative stress triggered in different pathways, such as advanced glycation end products (AGEs) formation via polyol, protein kinase C (PKC) and hexosamine biosynthesis

  • This study aims to determine the effects of coffee on AGEs formation and platelet aggregation in diabetic rats

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Summary

Introduction

Diabetes mellitus (DM) is a chronic metabolic disease characterized by hyperglycemia that affects 415 million people worldwide, with an estimate for the coming decades of 642 million new cases[1,2]. Complications resulting from chronic hyperglycemia during DM are caused by oxidative stress triggered in different pathways, such as advanced glycation end products (AGEs) formation via polyol, protein kinase C (PKC) and hexosamine biosynthesis. These oxidative changes alter genetic expressions that damage pancreatic β cells and induce insulin resistance[5,6,7,8]. The irreversible glycation of subendothelial collagen and other structural proteins changes vase structure and promotes vascular permeability and synthesis of proinflammatory cytokines, leading to diabetic complications such as macrovascular disorders[10,12,13]. Hyperglycemia has been reported to increase the propensity for platelets to aggregate and degranulate, leading to hypercoagulability[14,15,16]

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