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: 

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 (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.


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.


⦁ 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


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.


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.



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