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The Effect Of Antidiabetic Agent Glibenclamide And Meltformine On Lipids And Glycated Haemoglobin In Type 2 Diabetes Patient Attending Uith Ilorin
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2.1 EPIDEMIOLOGY AND ETIOLOGY OF TYPE 2 DIABETES (NIDDM)
Type 2 diabetes is the predominant form of diabetes and accounts for at least 90% of all cases of Diabetes mellitus (Gonzalez et al., 2009). The rise in prevalence is predicted to be much greater in developing than in developed countries (69 versus 20%) (Shaw et al., 2010). In developing countries, people aged 40 to 60 years (that is, working age) are affected most, compared with those older than 60 years in developed countries (Shaw et al., 2010). This increase in type 2 diabetes is inextricably linked to changes towards a Western lifestyle (high diet with reduced physical activity) in developing countries and the rise in prevalence of overweight and obesity (Chan et al., 2009; Charles, 2010). There are approximately 1.4 million people with diagnosed type 2 diabetes in the UK (Bennett et al., 1995). The incidence of diabetes increases with age, with most cases being diagnosed after the age of 40 years. This equates to a lifetime risk of developing diabetes of 1 in 10 (Neil et al., 1987). Type 2 diabetes is a heterogenous disorder caused by a combination of genetic factors related to impaired insulin secretion, insulin resistance and environmental factors such as obesity, over eating, lack of exercise, and stress as well as aging (Kaku, 2010). It is typically a multifactorial disease involving multiple genes and environmental factors to varying extents (Holt, 2004). Type 2 diabetes is the common form of idiopathic diabetes and is characterized by a lack of the need for insulin to prevent ketoacidosis. It is not an autoimmune disorder and the susceptible genes that predispose to NIDDM have not been identified in most patients. This could be due to the heterogeneity of the genes responsible for the susceptibility to NIDDM.
2.2 Pathogenesis of type 2 diabetes
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 as shown in Figure 2. The 100% concordance rate in identical twins is thought to be over-estimated, due to a selection or reporting bias. A population based twin study in Finland has shown a concordance rate of 40%, and environmental effect may be a possible reason for the higher concordance rate for type 2 Diabetes mellitus than for type 1 Diabetes mellitus (Kaprio et al., 1992). Type 2 Diabetes mellitus affects 1 to 2% of caucasians (Cook et al., 1993) but it is much higher in some ethnic groups such as Pima Indians (Knowler et al., 1990) and Arabs (Richens et al., 1988) and approaches 50% in South India. This indicates that genetic factors are more important than environmental factors. Except for maturity onset diabetes of the young (MODY), the mode of inheritance for type 2 Diabetes mellitus is unclear. MODY, inherited as an autosomal dominant trait, may result from mutations in glucokinase gene on chromosome 7p. Glucokinase is a key enzyme of glucose metabolism in beta cells and the liver (Froguel et al., 1993; Hattersley et al., 1992). MODY is defined as hyperglycemia diagnosed before the age of twenty-five years and treatable for over five years without insulin in cases where islet cell antibodies (ICA) are negative and HLA-DR3 and DR4 are heterozygous. MODY is rare in Caucasians, less than 1%, and more common in blacks and Indians, more than 10% of diabetics. Chronic complications in MODY were thought to be uncommon but later were found to be more common, indicating its heterogeneity. Considering MODY as a separate entity may masquerade its association with specific genetic diseases; and without a definite genetic marker, it should be treated as type 1 DM (Tattershall, 1991). Identification of a nonsense mutation in the glucokinase gene and its linkage with MODY was reported for the first time in a French family, implicating a mutation in a gene involved in glucose metabolism in the pathogenesis of type 2 Diabetes mellitus (Vionnet et al., 1992). Later, sixteen mutations were identified in 18 MODY families. They included 10 mutations that resulted in an amino acid substitution, 3 that resulted in the synthesis of truncated protein, and 3 that affected RNA processing. Hyperglycemia in these families was usually mild and began in childhood, whereas the hyperglycemia of MODY families without glucokinase mutations usually appearedafter puberty (Froguel et al., 1993). Molecular genetic studies in type 2 Diabetes mellitus, with the exception of MODY, have not been as successful as in type 1 Diabetes mellitus. Mutations in the insulin gene lead to the synthesis and secretion of abnormal gene products, leading to what are called insulinopathies (Gabbay, 1980). Most of the patients with insulinopathies have hyperinsulinemia, inherited in autosomal fashion, heterozygous for normal and mutant alleles, and normally respond to exogenous insulin administration. Al Homsi and Lukic (1992) explained that most insulin gene mutations lead to:
a. Abnormal insulins: such as insulins Chicago and Wakayama where the mutation leads to an amino acid replacement at an important site for receptor interaction or
b. The mutation may interfere in the proinsulin processing to insulin (Chan et al., 1987).
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ABSRACT - [ Total Page(s): 1 ]Abstract Is Coming Soon ... Continue reading---
APPENDIX A - [ Total Page(s): 1 ]APPENDIX IQUESTIONAIRE TO ACCESS THE ANTHROPOLOGIC INDICES OF PATIENTS WITH TYPE TWO DIABETES MELLITUS ON ANTIDIABETIC DRUGS (METFORMIN AND GLIBENCLAMIDE) ATTENDING UITH ILORIN.INTRODUCTION: I am a final year students of the Department of Medical Laboratory Science, School of Basic Medical Sciences, Kwara State University, Malete, Kwara State. This questionnaire is aimed at accessing the demographic indices of patients with type 2 Diabetes mellitus on metformin and diabinese in Ilorin metropolis ... Continue reading---
APPENDIX B - [ Total Page(s): 5 ]Step 2100µl of the supernatant was dispensed into the clean test tubes respectively.2ml of the cholesterol reagent was addedIt was incubated at room temperature for 10minsAbsorbance of sample against reagent blank was measured at 505nmGlycated HaemoglobinGlycated Haemoglobin is a form of haemoglobin that is measured primarily to identify the three-month average plasma glucose concentration. The test is limited to a three-month average.ProcedureReagentsBlank(µl) samp ... Continue reading---
CHAPTER ONE - [ Total Page(s): 2 ]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 PROBLEMTo know if antidiabetic agents glibenclamide and meltformine has any effect on lipid and glycated haemoglobin in type 2 diabetes patients1.3 AIM OF STUDYTo evaluate the effect of antidiabetic agent glibenclamide and meltformine on lipids and glycated haemoglobin in type 2 diabetes patient attendi ... Continue reading---
CHAPTER THREE - [ Total Page(s): 1 ]CHAPTER THREE3.1 Material and Method3.2 Study AreaThe study was carried out at University of Ilorin Teaching Hospital, Ilorin, Kwara State. The hospital is located at the State capital of Ilorin, Kwara State Nigeria. It is a referral center to other public and private hospitals within and outside the state.3.3 SAMPLE SIZE DETERMINATIONThere was a random selection of ninety (90) subjects, 60 were type 2 Diabetes mellitus individual using either one or combine antidiabetic agent (glibe ... Continue reading---
CHAPTER FOUR - [ Total Page(s): 4 ]Tables 4.6: Correlation of Duration in Diabetes and BMI with biochemical parameters (T. cholesterol, High Density Lipoprotein, Low Density Lipoprotein, triglycerides, glycated, and fasting blood sugar) in Diabetic patient using antidiabetic drugs (Metformin and Glianpride). ... Continue reading---
CHAPTER FIVE - [ Total Page(s): 2 ]CHAPTER FIVE5.0 DISCUSSIONThe study shows discrepant results about the influence of metformin on lipid profile (10). Some studies, in agreement with ours, reported reduction only in TC levels (Grant, 1996; Ginsberg et al., 1999), while others reported reduction of TC and TG with an increase of HDL-C (Robinson et al., 1998; Yki-Jarvinen et al., 1999). Still other studies showed no changes in lipid profile (Groop et al., 1998; Rains et al., 1998). Another investigation showed an association of met ... Continue reading---
REFRENCES - [ Total Page(s): 3 ]Rodger, W. (2012). Sulphonylureas and heart disease in diabetes management. Diabetes Spectrum. Pg. 12–27.Rosenbaum, M. and Leibel, R. L. (2014). Role of leptin in energy homeostasis in humans. Journal of Endocrinology. 223(1): 83-96.Rowley, D.E. and Bezold, D.C. (2012). Using new insulin strategies in the outpatient treatment of diabetes: clinical applications. Journal of American Medical Association. Pg. 289.Shaw, D., De Rosa, N. and Di Maro, G. (2010). Metformin improves glucose, lipid ... Continue reading---
