Experimental evidences suggest that hyperglycaemia-induced overproduction of reactive oxygen species and subsequent damage to proteins, lipids and DNA may play a key role in the development of distal symmetric polyneuropathy (DSPN)—the most common complication of diabetes mellitus. The study population consisted of 51 individuals aged 52–82 years classified into 3 groups: 16 patients diagnosed with type 2 diabetes mellitus (T2DM) with DSPN, 16 T2DM patients without DSPN and 19 control subjects without diabetes and neuropathy. The study was conducted to determine the activity of antioxidant enzymes: catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX) and total antioxidant status (TAS) in the examined groups. An alkaline comet assay was used to determine the extent of DNA damage of oxidized purines as glicosylo-formamidoglicosylase (Fpg) sites, and oxidized pyrimidines as endonuclease III (Nth) sites. A significant decrease of SOD (P < 0.05), GPX (P < 0.05) and nonsignificant decrease of CAT (P > 0.05), and TAS status (P > 0.05) were seen in T2DM patients with neuropathy compared to T2DM patients as well as controls. T2DM patients with or without neuropathy revealed significantly lower (P < 0.05) plasma concentration of nitrous oxide compared to the control subjects. Endogenous level of oxidative DNA damage in T2DM patients with DSPN was significantly higher compared both to the controls and T2DM patients without DSPN (P < 0.001). Moreover, lymphocytes isolated from T2DM patients with DSPN were more susceptible to oxidative DNA lesions induced by hydrogen peroxide than from T2DM patients without DSPN (P < 0.001). Our results confirm hypothesis that oxidative stress may play a substantial role in the development and progression of diabetic distal symmetric polyneuropathy.

Non-alcoholic fatty liver disease (NAFLD) is one of the most common pathologies of that organ. The development of the disease involves a variety of mechanisms, including insulin resistance, oxidative stress, endoplasmic reticulum stress, endotoxins from the intestinal flora and genetic predispositions. Additionally, clinical data suggest that the presence of NAFLD is associated with excessive activation of the immune system. For practical purposes, attention should be paid to the moment when the subjects predisposed to NAFLD develop inflammatory infiltration and signs of fibrosis in the liver (non-alcoholic steatohepatitis – NASH). Their presence is an important risk factor for hepatic cirrhosis, hepatic failure, and hepatocellular carcinoma, as well as for the occurrence of cardiovascular events. Regardless of the diagnostic methods used, including laboratory tests and imaging, liver biopsy remains the gold standard to identify and differentiate patients with NAFLD and NASH. The search for other, safer, cheaper and more readily available diagnostic tests is still being continued. Attention has been drawn to the usefulness of markers of immune status of the organism, not only for the diagnosis of NASH, but also for the identification of NAFLD patients at risk of disease progression. Despite the effectiveness of medication, no recommendations have been established for pharmacotherapy of NAFLD. Data indicate the primary need for non-pharmacological interventions to reduce body weight. However, there is evidence of the applicability of certain drugs and dietary supplements, which, by their effect on the immune system, inhibit its excessive activity, thus preventing the progression of NAFLD to NASH.

Background: Fibrin formation and structure may be affected by a plethora of factors, including both genetic and posttranslational modifications, such as glycation, nitration or acetylation. Methods: The present study examines the effect of fibrinogen glycation on fibrin polymerization, measured in fibrinogen concentration-standardized plasma of subjects with type 2 diabetes mellitus (T2DM) and in a solution of human fibrinogen exposed to 30 mM glucose for four days. Results: The fibrin polymerization velocity (Vmax) observed in the T2DM plasma (median 0.0056; IQR 0.0049‒0.0061 AU/s) was significantly lower than in non-diabetic plasma (median 0.0063; IQR 0.0058‒0.0071 AU/s) (p < 0.05). Furthermore, significantly lower Vmax was observed for glucose-treated fibrinogen (Vmax 0.046; IQR 0.022‒0.085 AU/s) compared to control protein incubated with a pure vehicle (Vmax 0.053; IQR 0.034‒0.097 AU/s) (p < 0.05). The same tendency was observed in the fibrinogen samples supplemented with 6 mM glucose just before measurements. It is assumed that glucose may affect the ability of fibrinogen to form a stable clot in T2DM subjects, and that this impairment is likely to influence the outcomes of some diagnostic assays. As the example, the impaired clotting ability of glycated fibrinogen may considerably influence the results of the standard Clauss method, routinely used to determine fibrinogen concentration in plasma. The stoichiometric analysis demonstrated that spontaneous glycation at both the sites with high and low glycation potential clearly dominated in T2DM individuals in all fibrinogen chains.

Metformin treatment in patients with different degrees of HF and T2DM is associated with a reduction in mortality and does not affect the hospitalisation rate.

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The incidence of nonalcoholic fatty liver disease (NAFLD) is growing worldwide. Epidemiological data suggest a strong relationship between NAFLD and T2DM. This is associated with common risk factors and pathogenesis, where obesity, insulin resistance and dyslipidemia play pivotal roles. Expanding knowledge on the coexistence of NAFLD and T2DM could not only protect against liver damage and glucotoxicity, but may also theoretically prevent the subsequent occurrence of other diseases, such as cancer and cardiovascular disorders, as well as influence morbidity and mortality rates. In everyday clinical practice, underestimation of this problem is still observed. NAFLD is not looked for in T2DM patients; on the contrary, diagnosis for glucose metabolism disturbances is usually not performed in patients with NAFLD. However, simple and cost-effective methods of detection of fatty liver in T2DM patients are still needed, especially in outpatient settings. The treatment of NAFLD, especially where it coexists with T2DM, consists mainly of lifestyle modification. It is also suggested that some drugs, including hypoglycemic agents, may be used to treat NAFLD. Therefore, the aim of this review is to detail current knowledge of NAFLD and T2DM comorbidity, its prevalence, common pathogenesis, diagnostic procedures, complications and treatment, with special attention to outpatient clinics.

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