Table of contents.
CHAPTER ONE
1.0
INTRODUCTION
1.1
BACKGROUND OF STUDY
1.2 STATEMENT OF PROBLEM
1.3 AIM OF STUDY
1.4 SPECIFIC OBJECTIVE
1.5 SIGNIFICANCE OF THE STUDY
1.6 RESEARCH HYPOTHESIS
CHAPTER TWO
LITERATURE REVIEW
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
2.3 Pathophysiology of type 2 diabetes (NIDDM)
2.4
LIPIDS
2.4.1 CHOLESTEROL
2.4.1.1 BIOSYNTHESIS
2.4.1.2 Regulation of
Cholesterol Synthesis
2.4.1.3 Metabolism,
Recycling and Excretion
2.4.2
Triglycerides
2.4.2.1
Chemical Structure of Triglyceride
2.4.2.2
Metabolism of Triglycerides
2.5 Glycated hemoglobin (hemoglobin A1c, HbA1c, A1C, or Hb1c;
sometimes also
2.5.1 Structure and function
2.5.3 Epimodility
2.5.4 Estimating HDL via associated cholesterol
2.7 Antidiabetic Agents
CHAPTER THREE
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
REFERENCE
APPENDIX I
APPENDIX II
CHAPTER ONE
1.0 INTRODUCTION
1.2
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 (Akinmokun et 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:
1. Obesity/overweight (especially excess visceral
adiposity)
2. Excess glucorticoids (cushing’s syndrome or
steroid therapy)
3. Excess growth hormone (acromegaly)
4. Pregnancy, gestational diabetes
5. Polycystic ovary disease
6. Lipodystrophy (acquired or genetic, associated
with lipid accumulation in liver)
7. Autoantibodies to the insulin receptor
8. Mutations of insulin receptor
9. Mutations of the peroxisome proliferators’
activator receptor γ (PPAR γ)
10. Mutations that cause genetic obesity (e.g.,
melanocortin receptor mutations)
11. 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 (Reaven et al., 2005). Metabolic syndrome is associated with a high
risk of coronary heart disease and premature mortality (Isomaa et 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 (Knowler et
al., 1990). Nearly 70-80% of the population with Diabetes mellitus is diagnosed with metabolic syndrome. Metformin
is a biguanide euglycemic agent, has been approved by the food and drug
administration for the treatment of type 2 Diabetes
mellitus
(Drouin et 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 (Penbe et 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 glycated haemoglobin in type 2
diabetes patients
1.3 AIM OF STUDY
To evaluate the effect of antidiabetic agent
glibenclamide and meltformine on lipids and glycated haemoglobin in type 2
diabetes patient attending UITH Ilorin.
1.4 SPECIFIC OBJECTIVE
·
To estimate
concentration of lipid and glycated haemoglobin in type 2 diabetes patient on
antidiabetic agents (glibenclamide and meltformine)
·
To examined lipid parameters and glycated haemoglobin 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.
Glycated haemoglobin results pattern will show
if the patients are adhering to the use of antidiabetic agents.
There will be a correlation between lipids and
glycated haemoglobin based on the use of antidiabetic agents.
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