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Abstract Diabetes mellitus (DM) is a syndrome with disordered metabolism and inappropriate hyperglycemia due to either a deficiency of insulin secretion or due to combination of insulin resistance and inadequate insulin secretion to compensate. It has multisystem effects on both biochemical and functional consequences. Type II diabetes, both defects exist i.e. combination of peripheral insulin resistance and inadequate insulin secretion by pancreatic beta cells. For example, all overweight individuals have insulin resistance, but diabetes develops only in those who cannot increase insulin secretion sufficiently to compensate for their insulin resistance. Their insulin concentrations may be high, yet inappropriately low for the level of glycemia. Rates of diabetes are increasing worldwide. The World Health Organization (WHO) has estimated that the global prevalence (for all age groups) would rise from 2.8% in 2000 to 4.4% in 2030. At least 171 million people currently have diabetes, and this figure is likely to more than double to 366 million by 2030. Diabetes mellitus is one of the main causes of microvascular (i.e., retinal, renal), macrovascular (i.e., coronary, peripheral vascular) and neuropathic complications. It also leads to end-stage renal disease (ESRD). Diet control is a basic part of management in every case. Treatment cannot be effective unless adequate attention is given to ensuring appropriate nutrition. Together with dietary treatment, a programme of regular physical activity and exercise should be considered for each person Helicobacter pylori (H. pylori) are a motile, flagellated, gram-negative, spiral bacterium (Lopes, 2010) which survives the acid environment of the stomach by producing the enzyme urease (McColl, 2010 and Lopes, 2010). The exact route of transmission of H. pylori is unknown; currently favored mechanisms appear to be gastro-oral and fecal-oral routes (Tan and Wong, 2011). Infection with H. pylori can lead to inflammation of the gastric mucosa with subsequent ulceration (McColl, 2010; Lopes, 2010 and Tan, 2011). Infection is a major cause of chronic gastritis, a condition that initiates the pathogenic sequence of events leading to atrophic gastritis, intestinal metaplasia, dysplasia and subsequently cancer (Kabir, 2009 and Lopes, 2010) Infection with H. pylori is a co-factor in the development of duodenal or gastric ulcers (develop in 1 to 10%), gastric cancer (in 0.1 to 3%) and gastric mucosa associated lymphoid tissue (gMALT) lymphoma (in <0.01%) (McColl, 2010). While the bacterium is not a direct cause of cancer, its presence and resultant reduction in acid production are necessary factors in causation (Lopes, 2010). The risk of these disease outcomes in infected patients varies widely among different populations and the great majority of patients with H. pylori will not have any clinically significant complications (McColl, 2010 and Lopes, 2010)The prevalence of H. pylori infection varies between countries; in Europe, the prevalence varies between 7 and 33% (Ford and Axon, 2010). Infection is usually acquired in childhood (Tan and Wong, 2011); in developing countries, the infection is typically acquired before 10 years of age, while in developed countries there is an age-related increase in prevalence (Tan, 2011 and McColl, 2010). The major risk factor for H. pylori infection is the socio-economic status of the family during childhood, in particular the level of sanitation and household hygiene (Steinstrom et al, 2008), however genetic susceptibility also appears to play a role (Tan and Wong 2011). The predominant genotype varies greatly between regions and accounts for some of the gastric cancer risk seen in some population groups, such as Japan and South Korea which tend to harbor more virulent strains (Tan and Wong, 2011).The role of screening and eradicating H. pylori in the general population and in targeted populations, as a means to reduce the incidence of gastric cancer is an area of much debate .There is growing evidence that adopting such an approach in populations at high risk of gastric cancer may reduce the future incidence of gastric cancer (Ford and Axon, 2010). Diabetes mellitus (DM) is one of the important causes of dyspepsia. Disordered gastrointestinal motor function is now recognized as a major cause of DM. Beside DM the H. pylori is also a well established cause of dyspepsia (Devrajani et al, 2010). The incidence of H. pylori is increased in DM (Saluja et al, 2002). Delayed gastric emptying and antral dysmotility are important causes of dyspepsia in diabetes. The role of H. pylori infection in diabetic dyspepsia is mainly related to blood glucose concentration. Hyperglycemia may induce the infection by H. pylori or the silent infection may get reactivated and produce symptoms of dyspepsia in diabetes (Devrajani et al, 2010). |