THE STUDY OF BIOCHEMICAL PARAMETERS AND EFFECT OF GLIBENCLAMIDE IN TYPE 2 DIABETES MELLITUS
Abstract
India is a country known for its rich and varied cultural heritage. It is also one of the oldest civilizations (Indus Valley Civilization) in the world. India is the seventh largest country in the world, divided into 29 states and 7 union territories (Figure 1). Since its independence from the British in 1947, India has achieved an all-round progress socio-economically. It is also self-sufficient in agricultural production and one of the emerging top industrialized countries of the world [1,2].
Knowledge of diabetes dates back to centuries before Christ. The Egyptian Ebers Papyrus [ca. 1500 B.C.] described an illness associated with the passage of much urine. Celsus [30 B.C. to 50 A.D.] recognised the disease but it was not until two centuries later that another Greek physician, the renowned Aretaeus of Cappadocia, gave the name diabetes [a siphon]. He made the first complete clinical description, describing it as "a melting down of the flesh and limbs into urine". In the 3rd to 6th centuries A.D., scholars in China, Japan and India wrote of a condition with polyuria in which the urine was sweet and sticky. However, although it had been known for centuries that diabetic urine tasted sweet, it remained for Willis in 1674 to add the observation "as if imbued with honey and sugar". The name diabetes mellitus [mellitus = honey] was thus established. A century after Willis, Dobson demonstrated that the sweetness was, indeed, due to sugar. From the time of the earliest recorded history of diabetes, progress in the understanding of the disorder came slowly until the middle of the 19th century [3] .
However, over these centuries gradually the course and complications of the disease were recognised. Gangrene had been described by Avicenna, an Arab physician, in about 1000 A.D. Its hereditary tendency was described ["Passed with the seed"] as well as two general varieties, one with the classic acute symptoms noted above [Type I or IDDM in today's terminology] and the other with "torpor, indolence and corpulence" [Type II or NIDDM]. Within the past century an association was established with a disturbance in the beta cells. These islets were first noted in fish by Brockman early in thel9th century, but they bear the name of Langerhans who described them in mammals in 1869. Soon after, the German scientists, von Mering and Minkowski, found that surgical removal of the pancreas produced diabetes in the dog. At the turn of the century, an American, Opie, noted the beta cells in the islets to be damaged in humans dying of the disease. Finally in 1921 Banting and Best, Canadians, prepared active extracts of pancreas which lowered the elevated glucose levels of diabetic dogs [4].
Type 2 diabetes mellitus is often characterized by hyperglycemia as a result of increased insulin resistance in hepatic, peripheral tissues and pancreatic ?-cell dysfunction. Approximately 92% of patients with type 2 diabetes mellitus demonstrate insulin resistance; however hyperglycemia is always a consequence of insulin deficiency. This study was done on 75 patients newly diagnosed diabetes type 2 characterized by dyslipidaemia that is increased triglycerides and decreased HDL. Hypoglycemia and weight gain are common problems with oral sulfonylurea drugs. In this study two different oral hypoglycemic drugs Glibenclamide (insulin secretagogues)) were used for treatment of patients with type 2 diabetes mellitus. The effects of these drugs on fasting and postprandial blood glucose levels, lipid profiles (TC, TG, and HDL) were studied. Two groups of newly diagnosed type 2 diabetic patients, group 1 (75 patients) were subjected to treatment with Glibenclamide (5 mg once daily), Fasting and postprandial blood glucose levels, lipid profiles (TC, TG, and HDL) were analysed for these patients before and after 90 days of oral hypoglycemic drug treatment. The results demonstrated that Glibenclamide has a greater postprandial glucose regulator. Glibenclamide produces greater percent reduction with respect to fasting blood glucose levels, postprandial blood glucose levels
Key words: Glibenclamide, lipid profile lipoprotein a and lipoprotein lipase Type 2 diabetes mellitus
