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TITLE PAGE

THE EFFECT OF ANTIDIABETIC AGENT GLIBENCLAMIDE AND MELTFORMINE ON LIPIDS AND GLYCATEDHAEMOGLOBIN IN TYPE 2 DIABETES PATIENT ATTENDING UITH ILORIN

BY

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EE/H2013/01430
DEPARTMENT OF ----
SCHOOL OF ---
INSTITUTE OF ---

DECEMBER,2018

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APPROVAL PAGE

This is to certify that the research work, "the effect of antidiabetic agent glibenclamide and meltformine on lipids and glycatedhaemoglobin in type 2 diabetes patient attending uith ilorin" by ---, Reg. No. EE/H2007/01430 submitted in partial fulfillment of the requirement award of a Higher National Diploma on --- has been approved.

By
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Supervisor                                                  Head of Department.
Signature……………….                           Signature……………….        

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External Invigilator

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DEDICATION
This project is dedicated to Almighty God for his protection, kindness, strength over my life throughout the period and also to my --- for his financial support and moral care towards me.Also to my mentor --- for her academic advice she often gives to me. May Almighty God shield them from the peril of this world and bless their entire endeavour Amen.

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ACKNOWLEDGEMENT

The successful completion of this project work could not have been a reality without the encouragement of my --- and other people. My immensely appreciation goes to my humble and able supervisor mr. --- for his kindness in supervising this project.
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TABLE OF CONTENT
COVER PAGE
APPROVAL PAGE
DEDICATION
ACKNOWLEDGEMENT
TABLE OF CONTENT

• INTRODUCTION
• BACKGROUND AND ITS OPERATION
• STATEMENT OF THE PROBLEM
• AIM OF STUDY
• SPECIFIC OBJECTIVE
• SIGNIFICANCE OF THE STUDY
• RESEARCH HYPOTHESIS

CHAPTER TWO
2.0     INTRODUCTION
2.1    EPIDEMIOLOGY AND ETIOLOGY OF TYPE 2 DIABETES (NIDDM)
2.2    PATHOGENESIS OF TYPE 2 DIABETES
2.3     ENVIRONMENTAL FACTORS IN THE PATHOGENESIS OF TYPE 2 DIABETES
2.4     PATHOPHYSIOLOGY OF TYPE 2 DIABETES (NIDDM)
2.5     LIPIDS
2.6     GLYCATED HEMOGLOBIN (HEMOGLOBIN A1C, HBA1C, A1C, OR HB1C
2.7     HDL
2.8     ANTIDIABETIC AGENTS

CHAPTER THREE
METHODOLOGY
3.1     MATERIAL AND METHOD
3.2     STUDY AREA
3.3     SAMPLE SIZE DETERMINATION
3.4     COLLECTION OF SAMPLE
3.5     MEASUREMENT OF VARIABLES
3.6     STATISTICAL ANALYSIS
3.7     ETHICAL CONSIDERATION AND INFORMED CONSENT      

CHAPTER FOUR
4.0     RESULTS

CHAPTER FIVE
5.0     DISCUSSION
5.1     CONCLUSION
5.2     RECOMMENDATION 

CHAPTER ONE
1.0  INTRODUCTION

• BACKGROUND OF STUDY

Diabetes mellitus (DM) has been defined as a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both (Akinmokunet al.,1992). Insulin is a hormone produced in pancreas and enables body cells to absorb glucose that is converted into energy when the body is in need. If the body cell does not absorb the glucose, it will accumulate in the blood causing "hyperglycemia”, chronic hyperglycemia however leads to various potential complication (Pasquali, 2000).
Under normal physiological conditions, plasma glucose concentrations are maintained within a narrow range, despite wide fluctuations in supply and demand, through a tightly regulated and dynamic interaction between tissue sensitivity to insulin (especially in liver) and insulin secretion (DeFronzo and Goodman, 1995). In type 2 diabetes these mechanisms break down, with the consequence that the two main pathological defects in type 2 diabetes are impaired insulin secretion through a dysfunction of the pancreatic β-cell, and impaired insulin action through insulin resistance (Holt, 2004). Type 2 Diabetes mellitus has a greater genetic association than type 1 DM, the pathogenesis of type 2 Diabetes mellitus is characterized by impaired insulin secretion and insulin resistance.Some causes of insulin resistance are:

• Obesity/overweight (especially excess visceral adiposity)
• Excess glucorticoids (cushing’s syndrome or steroid therapy)
• Excess growth hormone (acromegaly)
• Pregnancy, gestational diabetes
• Polycystic ovary disease
• Lipodystrophy (acquired or genetic, associated with lipid accumulation in liver)
• Autoantibodies to the insulin receptor
• Mutations of insulin receptor
• Mutations of the peroxisome proliferators’ activator receptor γ (PPAR γ)
•  Mutations that cause genetic obesity (e.g., melanocortin receptor mutations)
• Hemochromatosis (a hereditary disease that causes tissue iron accumulation) (Guyton and Hall, 2006).         

The metabolic syndrome (MS), or insulin resistance syndrome accommodates the clustering together of certain cardiovascular risk factors associated with insulin resistance and hyperinsulinemia (Campbell, 2005). It was first identified in 1988 by Gerald Reaven, a Stanford University endocrinologist, in a lecture to the American Diabetes Association. At various times, this syndrome has been called dysmetabolic syndrome, insulin resistance syndrome or syndrome X. Now simply known as metabolic syndrome (Reavenet al., 2005).  Metabolic syndrome is associated with a high risk of coronary heart disease and premature mortality (Isomaaet al., 2001). Besides resulting in macrovascular complications, there is growing evidence that metabolic syndrome, like Diabetes mellitus, causes micro vascular complications in patients with type 2 Diabetes mellitus (Knowleret al., 1990). Nearly 70-80% of the population with Diabetes mellitus is diagnosed with metabolic syndrome. Metformin is a biguanideeuglycemic agent, has been approved by the food and drug administration for the treatment of type 2 Diabetes mellitus (Drouinet al., 2004). Although metformin is as effective as sulfonylureas, the drug differs in several respects: Metformin reduces insulin resistance without directly affecting insulin secretion, causes weight loss rather than weight gain, and has lactic acidosis rather than hypoglycemia as its most serious side effect (Kaku, 2010). Glibenclamide is a second-generation sulfonylurea drug. It is at least as effective as the first-generation agents and is effective in doses that are considerably less than those needed with first generation sulfonylureas (Charles ,2010). It is a useful medication for patients with type 2 diabetes whose hyperglycemia is not adequately reduced by dietary management and exercise. It can be used as the initial drug in these patients or as the replacement drug for those with primary or secondary failure during therapy with first generation sulfonylureas (Charles, 2010). Side effects are minimal, and the most important is hypoglycemia. Although no difference persists between the treatment groups for total-cholesterol, triglycerides, HDL-cholesterol, and LDL-cholesterol, the antidiabetic agents seem to lower serum lipids most effectively, which may help prevent coronary events in T2DM patient (Penbeet al.,2003).
The present study was designed to investigate and compare the effects of glibenclamide and metformin on prevalence of metabolic syndrome in type 2 diabetic patients.

1.2    STATEMENT OF PROBLEM
To know if antidiabetic agents glibenclamide and meltformine has any effect on lipid and glycatedhaemoglobin in type 2 diabetes patients

1.3     AIM OF STUDY
To evaluate the effect of antidiabetic agent glibenclamide and meltformine on lipids and glycatedhaemoglobin in type 2 diabetes patient attending UITH Ilorin.
1.4     SPECIFIC OBJECTIVE

• To estimate concentration of lipid and glycatedhaemoglobin in type 2 diabetes patient on antidiabetic agents (glibenclamide and meltformine)
• To examined lipid parameters and glycatedhaemoglobin in pairs for their correlations for each study group.
• To compare the results obtained between the two groups

1.5 SIGNIFICANCE OF THE STUDY
This study showed the effect of two different antidiabetic agents (glibenclamide and meltformine) on lipid parameters and effect of long term management of type 2 Diabetes mellitus patients.

1.6 RESEARCH HYPOTHESIS
Plasma fasting lipid parameters will show no significant difference in both antidiabetic agents.
Glycatedhaemoglobin results pattern will show if the patients are adhering to the use of antidiabetic agents.

There will be a correlation between lipids and glycatedhaemoglobin based on the use of antidiabetic agents.

1.7                                                         PROJECT ORGANISATION
The work is organized as follows: chapter one discuses the introductory part of the work,   chapter two presents the literature review of the study,  chapter three describes the methods applied,  chapter four discusses the results of the work, chapter five summarizes the research outcomes and the recommendations.

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