IntroductionType II diabetes mellitus (T2DM) is a metabolic disorder that poses a serious health concern worldwide due to its rising prevalence. Hypertension (HT) is a frequent comorbidity of T2DM, with the co-occurrence of both conditions increasing the risk of diabetes-associated complications. Inflammation and oxidative stress (OS) have been identified as leading factors in the development and progression of both T2DM and HT. However, OS and inflammation processes associated with these two comorbidities are not fully understood. This study aimed to explore changes in the levels of plasma and urinary inflammatory and OS biomarkers, along with mitochondrial OS biomarkers connected to mitochondrial dysfunction (MitD). These markers may provide a more comprehensive perspective associated with disease progression from no diabetes, and prediabetes, to T2DM coexisting with HT in a cohort of patients attending a diabetes health clinic in Australia.MethodsThree-hundred and eighty-four participants were divided into four groups according to disease status: 210 healthy controls, 55 prediabetic patients, 32 T2DM, and 87 patients with T2DM and HT (T2DM+HT). Kruskal-Wallis and χ2 tests were conducted between the four groups to detect significant differences for numerical and categorical variables, respectively.Results and discussionFor the transition from prediabetes to T2DM, interleukin-10 (IL-10), C-reactive protein (CRP), 8-hydroxy-2’-deoxyguanosine (8-OHdG), humanin (HN), and p66Shc were the most discriminatory biomarkers, generally displaying elevated levels of inflammation and OS in T2DM, in addition to disrupted mitochondrial function as revealed by p66Shc and HN. Disease progression from T2DM to T2DM+HT indicated lower levels of inflammation and OS as revealed through IL-10, interleukin-6 (IL-6), interleukin-1β (IL-1β), 8-OHdG and oxidized glutathione (GSSG) levels, most likely due to antihypertensive medication use in the T2DM +HT patient group. The results also indicated better mitochondrial function in this group as shown through higher HN and lower p66Shc levels, which can also be attributed to medication use. However, monocyte chemoattractant protein-1 (MCP-1) levels appeared to be independent of medication, providing an effective biomarker even in the presence of medication use. The results of this study suggest that a more comprehensive review of inflammation and OS biomarkers is more effective in discriminating between the stages of T2DM progression in the presence or absence of HT. Our results further indicate the usefulness of medication use, especially with respect to the known involvement of inflammation and OS in disease progression, highlighting specific biomarkers during disease progression and therefore allowing a more targeted individualized treatment plan.
Oxidative stress (OS) has been shown to have a negative effect on the autonomic nervous system (ANS) and on ANS modulation of heart rate. Mitochondrial ATP production is the main source of reactive oxygen species (ROS) and hence the regulation of ROS becomes an important issue in maintaining optimal ANS functionality. Humanin (HN), a mitochondrial-derived peptide, plays an important role in lowering OS. Sympathovagal balance was assessed in 124 healthy participants through heart rate variability (HRV) analysis and compared across changes in HN concentrations divided into quintiles, with values of HN ranging from 64.6 to 343.2 pg/mL.Significant differences included various frequency domain and nonlinear HRV parameters, particularly between first and fourth HN quintiles with p values < 0.001 for recurrence plot analysis (RPA), detrended fluctuation analysis (DFA) a1 and Poincaré plot ratio SD1/SD2. The results revealed non-monotonic relationships between measures of HRV and HN concentration. A mitohormetic type of relationship was observed with HRV features increasing and then decreasing with increasing HN concentration. These results are consistent with previous findings of the importance of HN levels in regulating OS and extend these by revealing a concomitant effect on the modulation of cardiac rhythm by the ANS.
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