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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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Triglycerides as major components of very low-density lipoprotein (VLDL) and chylomicrons, play an important role in metabolism as energy sources and transporters of dietary fat. They contain more than twice as much energy (approximately 9kcal/g or 38kj/g) as carbohydrates (approximately 4kcal/g or 17kj/g) (Brefere et al., 2014).
2.5 Glycated hemoglobin (hemoglobin A1c, HbA1c, A1C, or Hb1c; sometimes also referred to as being Hb1c or HGBA1C) is a form of hemoglobin that is measured primarily to identify the three-month average plasma glucose concentration The test is limited to a three-month average because the lifespan of a red blood cell is four months (120 days). However, since RBCs do not all undergo lysis at the same time, HbA1C is taken as a limited measure of 3 months. It is formed in a non-enzymatic glycation pathway by hemoglobin's exposure to plasma glucose (Miedema, 2005).
HbA1c is a measure of the beta-N-1-deoxy fructosyl component of hemoglobin.[1] The origin of the naming derives from Hemoglobin type A being separated on cation exchange chromatography. The first fraction to separate, probably considered to be pure Hemoglobin A, was designated HbA0, the following fractions were designated HbA1a, HbA1b, and HbA1c, respective of their order of elution. There have subsequently been many more sub fractions as separation techniques have improved (Gerstein et al., 2008). Normal levels of glucose produce a normal amount of glycated hemoglobin. As the average amount of plasma glucose increases, the fraction of glycated hemoglobin increases in a predictable way. This serves as an indicator that blood sugar is increasing and that action should be taken.
In Diabetes mellitus, higher amounts of glycated hemoglobin, indicating poorer control of blood glucose levels, have been associated with cardiovascular disease, nephropathy, neuropathy, and retinopathy. A trial on a group of patients with Type 1 diabetes found that monitoring by caregivers of HbA1c led to changes in diabetes treatment and improvement of metabolic control compared to monitoring only of blood or urine glucose (Manley et al., 2004). However, a trial designed specifically to determine whether reducing HbA1c below the normal 6%, using primarily insulin and sulfonylureas (both known to easily drive blood sugar too low), would reduce the rate of cardiovascular events in type 2 diabetes found higher mortality—the trial was terminated early. The negative outcomes may well have been a result of the treatment approach, primarily insulin and sulfonylureas, utilized in the "intensive" treatment group instead of LCHF, GlP-1 analogues &SGLT-2 inhibitors, none of which have these problems & lower cardiovascular mortality(Sidorenkov et al., 2011).
2.5.1 Structure and function
HDL is the smallest of the lipoprotein particles. It is the densest because it contains the highest proportion of protein to lipids. Its most abundant apolipoproteins are apo A-I and apo A-II. A rare genetic variant, ApoA-1 Milano, has been documented to be far more effective in both protecting against and regressing arterial disease; atherosclerosis. The liver synthesizes these lipoproteins as complexes of apolipoproteins and phospholipid, which resemble cholesterol-free flattened spherical lipoprotein particles, whose NMR structure was recently published; the complexes are capable of picking up cholesterol, carried internally, from cells by interaction with the ATP-binding cassette transporter A1 (ABCA1). A plasma enzyme called lecithin-cholesterol acyltransferase (LCAT) converts the free cholesterol into cholesteryl ester (a more hydrophobic form of cholesterol), which is then sequestered into the core of the lipoprotein particle, eventually causing the newly synthesized HDL to assume a spherical shape. HDL particles increase in size as they circulate through the bloodstream and incorporate more cholesterol and phospholipid molecules from cells and other lipoproteins, for example by the interaction with the ABCG1 transporter and the phospholipid transport protein (PLTP) (Drzewoski et al., 1999).
HDL transports cholesterol mostly to the liver or steroidogenic organs such as adrenals, ovary, and testes by both direct and indirect pathways. HDL is removed by HDL receptors such as scavenger receptor BI (SR-BI), which mediate the selective uptake of cholesterol from HDL. In humans, probably the most relevant pathway is the indirect one, which is mediated by cholesteryl ester transfer protein (CETP). This protein exchanges triglycerides of VLDL against cholesteryl esters of HDL. As the result, VLDLs are processed to LDL, which are removed from the circulation by the LDL receptor pathway. The triglycerides are not stable in HDL, but are degraded by hepatic lipase so that, finally, small HDL particles are left, which restart the uptake of cholesterol from cells.
The cholesterol delivered to the liver is excreted into the bile and, hence, intestine either directly or indirectly after conversion into bile acids. Delivery of HDL cholesterol to adrenals, ovaries, and testes is important for the synthesis of steroid hormones.
Several steps in the metabolism of HDL can participate in the transport of cholesterol from lipid-laden macrophages of atherosclerotic arteries, termed foam cells, to the liver for secretion into the bile. This pathway has been termed reverse cholesterol transport and is considered as the classical protective function of HDL toward atherosclerosis.
However, HDL carries many lipid and protein species, several of which have very low concentrations but are biologically very active. For example, HDL and its protein and lipid constituents help to inhibit oxidation, inflammation, activation of the endothelium, coagulation, and platelet aggregation. All these properties may contribute to the ability of HDL to protect from atherosclerosis, and it is not yet known which are the most important. In addition, a small subfraction of HDL lends protection against the protozoan parasite Trypanosoma brucei brucei. This HDL subfraction, termed trypanosome lytic factor (TLF), contains specialized proteins that, while very active, are unique to the TLF molecule.
In the stress response, serum amyloid A, which is one of the acute-phase proteins and an apolipoprotein, is under the stimulation of cytokines (interleukin 1, interleukin 6), and cortisol produced in the adrenal cortex and carried to the damaged tissue incorporated into HDL particles. At the inflammation site, it attracts and activates leukocytes. In chronic inflammations, its deposition in the tissues manifests itself as amyloidosis (Lida et al., 2003)
It has been postulated that the concentration of large HDL particles more accurately reflects protective action, as opposed to the concentration of total HDL particles. This ratio of large HDL to total HDL particles varies widely and is measured only by more sophisticated lipoprotein assays using either electrophoresis (the original method developed in the 1970s) or newer NMR spectroscopy methods), developed in the 1990s.
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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---
