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Background and Objectives: Diabetes mellitus (DM) is a group of metabolic disorders of carbohydrate metabolism in which glucose is underutilized, producing hyperglycemia. Furthermore, it is proposed that the underutilization of glucose is associated with changes in the lipid profile. Changes in lipid profiles are also well related to the severity of DM. This study involved 50 were patients admitted with a diagnosis of DM; blood samples were drawn under aseptic precautions from cases of DM and healthy controls. Necessary investigations were carried out and values were tabulated for cases and controls separately for statistical evaluation. Our Results show that the DM patients compared to controls significant increase in the following parameters were observed. Cholesterol ratios increased. Furthermore, the levels of triacylglycerol increased. We conclude that there is a statistically significant large effect in cholesterol and TG a level of cases compared with controls, cholesterol level is increased and TG levels were well associated with blood sugar also increased .

Background: Helicobacter pylori, a member of Epsilonproteobacteria, is a Gram-negative microaerophilic bacterium that colonizes gastric mucosa of about 50% of the human population. Although most infections caused by H. pylori are asymptomatic, the microorganism is strongly associated with serious diseases of the upper gastrointestinal tract such as chronic gastritis, peptic ulcer, duodenal ulcer, and gastric cancer, and it is classified as a group I carcinogen. The prevalence of H. pylori infections varies worldwide. prevalence among middle-aged adults is over 80 percent in many developing countries, as compared with 20 to 50 percent in industrialized countries. The infection is acquired by oral ingestion of the bacterium and is mainly transmitted within families in early childhood, Humans can also become infected with Helicobacter heilmannii, a spiral bacterium found in dogs, cats, pigs, and nonhuman primates. Conclusion: H. pylori infection stimulates the reaction of autoantibodies with gastric epithelial cells, and this leads to gastritis. These autoantibodies can be directly induced to epithelial cells by activating complement, inducing apoptosis or provoking an antibody-dependent cytotoxic reaction resulting in subsequent tissue destruction.