Oxidative DNA damage and oxidized low density lipoprotein in Type II diabetes mellitus among patients with Helicobacter pylori infection

Abstract

BackgroundHelicobacter pylori (H. pylori) infection is reported to be associated with various extragastrointestinal conditions such as insulin resistance, diabetes mellitus and metabolic syndrome. H. pylori infection and type 2 diabetes mellitus (T2DM) are associated with oxidative stress, this cross-relation between H. pylori induced infection in T2DM and oxidative damage is still debated. Thus, the question arises whether an increase in the serum level of 8-OHdG and Ox-LDL will occurs in patients with T2DM infected H. pylori; this will be through determination and compare frequency of H. pylori infection in T2DM and non-diabetic patients.Methods100 patients presented with history of epigastric discomfort for more than 1 month; 50 patients with T2DM and 50 non-diabetics. Anti-H. pylori IgG using ELISA, fasting and postprandial glucose level, glycated hemoglobin (HbA1c) and body mass index (BMI) was calculated. Serum 8-OHdG and Ox-LDL was measured using ELISA for the 100 patients and 50 control subject.ResultsRates of H. pylori infection of T2DM and non-diabetic were 66 and 58 %, respectively, (p = 0.001). H. pylori IgG antibody was not correlated with HbA1c either in T2DM (p = 0.06) or non-diabetic (p = 0.25). Serum 8-OHdG level in T2DM with positive H. pylori infection showed a significant difference compared to non-diabetics with positive H. pylori infection (p = 0.001) and higher than that in T2DM with negative H. pylori. A correlation between 8-OHdG concentration and HbA1c in T2DM patients infected with H. pylori was observed (r = 0.39, p = 0.02). Serum Ox-LDL level in T2DM with positive H. pylori infection showed a significant difference compared to diabetics with both negative H. pylori infection and in non-diabetics with positive H. pylori infection (p = 0.001).ConclusionsIncreased levels of oxidative DNA damage (8-OHdG) and Ox-LDL suggest the mechanistic link between H. pylori infection combined with diabetes and increased generation of ROS and could play as an important image for high risk to atherosclerosis.

Helicobacter Pylori Infection Associated Diseases – A Systematic Review

“…In addition, 8-OHdG levels of these HPI non-diabetics were also higher than that of type 2 diabetes mellitus with negative H. pylori. These results showed a pathogenic linkage between HPI and diabetes [74] . There were significant differences of fasting blood glucose, high-density lipoprotein cholesterol between HPI patients and healthy controls [75] .…”

“…pylori infection is reported to be associated with insulin resistance, diabetes mellitus and metabolic syndrome [74][75][76] . Compared to non-diabetics with HPI, the levels of oxidative DNA damage (8-OHdG) in type 2 diabetes mellitus could be much higher (p = 0.001).…”

Helicobacter pylori infection and extragastric diseases in 2017

“…On the contrary, another recent study published by Nasif et al . reported increased levels of oxidative DNA damage and oxidized low‐density lipoproteins (ox‐LDL) in T2 DM with positive H. pylori infection compared to H. pylori ‐negative DM and no H .…”

Monitoring of cytogenetic effects in tick-borne encephalitis patients with type 2 diabetes mellitus, depending on polymorphism of glutathione-S-transferase genes

“…Кроме того, показано, что повышенный риск развития СД 2 типа (СД2) зависит от полиморфизма генов глутатион-S-трансфераз, в особенности от носительства в генотипе больного нефункционирующих из-за делеции вариантов генов GSTM1 и GSTT1, что приводит к нарушению синтеза одной из важнейших групп ферментов антиоксидантной защиты [4]. Показано, что развитие у больных СД2 инфекционного процесса и/или действие дополнительных мутагенных факторов также могут сопровождаться существенной активацией окислительного стресса и связанной с ним цитогенетической нестабильностью [5]. Известно, что некоторые инфекционные заболевания, такие как лихорадка Западного Нила, как правило, протекают в клинически более тяжелой форме у больных, имеющих СД2 как фоновое заболевание [6,7].…”