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Type 2 Diabetes Mellitus (T2DM) is influenced by the action of both hereditary and environmental factors. These factors are comprehended in the disease interaction with β cells and insulin sensitivity to the receptors.The main cause of T2DM development is ageing, obesity, and oxidative stress. The dysfunction of the β cells of the pancreas leads to insulin insensitivity in the liver, muscle and fat metabolism. These occur due to the result of oxidative stress. Lipid peroxidation is a key initiating factor in the development of oxidative stress, which results in T2DM and its related micro-and macro-vascular problems. These are initially compensated for the generation of excess insulin synthesis, thus ensuring normal glucose tolerance. When these compensatory processes are disrupted, the majority of persons develop T2DM. Although the gene is the primary cause of T2DM, the environment also plays an important role in the disease's progression. Particularly, a sedentary lifestyle characterised by excessive food consumption and physical inactivity is a known risk factor for obesity and type 2 diabetes. This review has briefly discussed the significance of numerous causal factors, and genomic and biochemical pathways which are responsible for increasing the production of oxidative stress, a crucial component for the etiology and development of T2DM. The conclusion drawn was that the analysis of oxidative stress markers may be one of the potential methods for the diagnosis and prognosis of T2DM. Furthermore, this review will be helpful to establish the broaden conceptual framework for future studies on oxidative stress with relation to etiology of type 2 diabetes and therapeutic development. [ABSTRACT FROM AUTHOR]

Background: Tuberculosis (TB) control is challenging due to failure of drug compliance and resistance. Mycobacterial antigen-induced cytokine secretions are helpful in detecting Mycobacterium tuberculosis infection and to determine prediction for the fate of TB infection and its cure. Considering immunological response to be a crucial factor in pathogenesis and cure of TB, it can be explored to determine clinical prospects in different categorical tubercular infections. This study was designed to compare serum levels of inflammatory (tumor necrosis factor [TNF]-alpha and interferon [IFN]-gamma) and anti-inflammatory cytokines/chemokines (interleukin [IL]-10 and IL-8) among different TB groups (freshly diagnosed, relapse, cases on antitubercular treatment [ATT], and healthy controls)., Methods: This cross-sectional study included total 100 subjects. The study subjects were further divided into four study groups with 25 cases in each of freshly diagnosed TB, TB relapse cases, cases on ATT, and 25 healthy controls. Levels of serum cytokines/chemokines (TNF-alpha, IFN-gamma, IL-10, and IL-8) were measured by flow cytometry., Results: Data analysis observed statistically significant differences in serum levels of TNF-alpha and IFN-gamma among the studied groups with significantly low levels in subjects on ATT and markedly high levels in TB relapse subjects. No statistically significant difference was observed in IL-10 and IL-8 levels. However, subjects with relapse revealed low IL-8 and high IL-10 levels., Conclusion: TNF-alpha and IFN-gamma have important roles in immune response and might be considered as indicators for response to ATT. However, high levels of IL-10 with low IL-8 appear to be associated with poor outcome and possibility of relapse., Competing Interests: None