الفهرس 
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Abstract
Diabetes is one of the most prevalent metabolic disorders globally and in recent decades the prevalence of diabetes in adults has increased. (Shaw et al., 2010)
Type 2 Diabetes Mellitus is a genetic disease. There are many genes involved, most of which have not as yet been identified. These genes control a number of chemical steps in β cell action, insulin secretion, insulin action at the cell level, insulin receptor production by the cell, and insulin action inside the cell. A different gene controls enzyme production for each step in this process. A defect in any one of glucose these genes can prevent enzyme production and block the action of insulin. This block can interfere with glucose uptake by the cell, increase glucose production by the liver, prevent uptake of and fatty acids by the fat cells, increase breakdown of the triglycerides, and cause many other metabolic defects. Thus, it is difficult to understand the pathophysiology of such a multifactorial disease. (Shoback DG. et al., 2011)
Progressive insulin deficiency is the other defect of T2DM. It is different than the insulin deficiency of T1DM in that it is not mediated by the immune system. The insulin deficiency may be due to β cell exhaustion from the hypersecretion of insulin, glucose and lipid toxicity to the β cells, or genetic factors. In all probability it is a combination of all these factors and the importance of each one may be different in different individuals. (Linnemann AK. et al., 2014)
• Method: It was conducted on twenty newly diagnosed Diabetic patients and twenty healthy individuals as control.
• Patients: were attending Minia University Hospital at outpatient diabetes clinic in October 2018.
The selected subjects included in the study were divided into two groups.
• group । (control group) : It included twenty healthy individuals for age and sex, 13 males and 7 females, their ages ranged from 17 to 53 years old
• group ॥ (diabetic group): It included twenty newly diagnosed Diabetic patients; 14 males and 6 females, their ages ranged from 18 to 68 years old.
Blood sampling;
About 5 ml of venous blood were withdrawn from each subject by using a disposable plastic syringe after sterilization of skin with iso propyl alcohol (70%) swaps. The next morning and under fasting condition for ten hours another 5 ml of venous blood were withdrawn from each subject as previously. Those samples were divided as follows;
• Four ml of blood was evacuated in Ethylene Diamine tetra acetic Acid (EDTA) containing tube for CBC, Flow Cytometric analysis and HbA1c.
• One ml was evacuated on plain tube. Blood was left to clot in the incubator then centrifuged. The expressed serum was used for determination of serum Glucose.
• The blood which was withdrawn under fasting condition was evacuated on plain tube. Blood was left to clot in the incubator then centrifuged. The expressed serum was used for determination of serum Cholesterol, serum LDL, Serum HDL and Serum T.G.
Results: our study shows significant increase in HbA1c in diabetic group to control group, shows significant rising in lipid profile (total cholesterol, LDL and Triglycerides) in diabetic group to control group except HDL which decreased in diabetic group to control group.
Our study also shows significant increase in CD4, CD8 and CD31 in diabetic group to control group.
And finally shows significant increase in WBCs count and Lymphocytes percentage in diabetic group to control group.
These results were caused by elevated blood glucose levels, and glucose molecules bind to hemoglobin in red blood cells. The more drawn out hyperglycemia proceeds in blood, the more glucose joins to hemoglobin in the red platelets and the higher the glycated hemoglobin. When a hemoglobin molecule is glycated, it remains that way. (Oliwia Witczak et al., 2014)
High blood triglycerides are usually associated with low HDL cholesterol, which is also a hallmark of plasma lipid abnormalities observed in diabetic patients. The group of lipid abnormalities related with T2DM is characterized by a little concentration of HDL cholesterol, minor dense LDL and a great concentration of TG. On the other hand, the relationship between lower HDL cholesterol levels and a higher risk of heart disease is well known regardless of TG levels and other risk factors. (Bitzur R. et al., 2009)
An elevated peripheral CD4 + T cell count may result from increased proliferation of CD4 + T cells. Suggesting that poor glycemic control may be one of the causes for severe infection among patients with T2DM. (Schuetz P. et al., 2011)
Therefore, it is likely that CD8+ cells have a distinguished role in the inflammatory status that is related to metabolic syndrome. Certainly, some CD8+ cell-derived cytokines, such as TNFα, are significantly raised in a metabolic syndrome scenario. (Pilatz, A. et al., 2017)
Hyperglycemia stimulates coagulation mechanism by increasing release of prothrombotic molecules like vWF and tissue factor, while inhibits fibrinolysis by raising PAI-1 concentration. (Boden G. et al., 2007)
Moreover, platelets are distinguished by raised expression of adhesion molecules in T2DM. Platelets of T2DM patients have raised expression of platelet activation markers (CD62P, CD31, CD49b and CD63) as compared to healthy individuals. (Ghoshal K. et al., 2014)
There is an association between white blood cells and diabetes, due to an excess in inflammatory mediators. Inflammatory agents, insulin, and human blood components are an important signal for any abnormalities that cause foreign agent invasion and / or inflammation. (Ohshita K. et al., 2004)
The inflammatory process within the diabetes is mediated by proinflammatory cytokines, reactive oxygen species, growth factors, and metalloproteinase; these are produced from leukocytes (neutrophils, lymphocytes, and macrophages) infiltrating the renal tissues. The homing of leukocytes into renal tissues is probably mediated by intercellular adhesion molecule-1 and the chemokines CX3CL1 and CCL2 and this process explain the increase of lymphocytes percentage in T2DM. (Galkina E. and Ley K. et al., 2006).