Iron overload is increasingly being connected to insulin resistance in Type 2 Diabetes Mellitus (T2DM) patients. Free iron causes the assembly of reactive oxygen species that invariably steer the body’s homeostasis towards oxidative stress-mediated diabetic complications. This study aims to assess the serum iron, total iron binding capacity (TIBC), and percentage transferrin saturation (Tsat) of 150 subjects divided into three groups (I,II,III) of 50. Healthy individuals (controls) constituted Group I. Group II consisted of T2DM patients with optimal glycaemic control. T2DM patients with suboptimal glycaemic control formed group III. Mean serum free iron concentration was 105.34 ± 3.5, 107.33 ± 3.45, and 125.58 ± 3.45 μg/dL in Group I, Group II, and Group III, respectively. Mean serum TIBC concentration in Group I, Group II, and Group III was 311.39 ± 5.47, 309.63 ± 6.1, and 284.2 ± 3.18 μg/dL, respectively. Mean serum transferrin saturation (%) in Group I, Group II, and Group III was 34.17 ± 1.21, 35.02 ± 1.2, and 44.39 ± 1.07, respectively. The difference between TIBC, mean serum free iron concentration, and transferrin saturation between Group I and Group III (for all, p values <0.001), as well as between Group II and Group III (p values 0.0012, 0.0015, and <0.0001, respectively) was statistically significant. The fasting plasma glucose values of Groups II and III were significantly higher than those of Group I, (p < 0.0001). Glycated haemoglobin (HbA1c) values were also shown to increase from Group I to II and then III, and the increase was highly significant (all p values <0.0001). Thus, decreased glycaemic control and an increase in the glycation of haemoglobin was the key to elevation in serum iron values and alterations in other parameters. However, a significant correlation was absent between serum iron and HbA1c (r = 0.05) and transferrin saturation (r = 0.0496) in Group III.

Background: Forkhead box P3 (FOXP3), a transcription factor is thought to be the master regulator of regulatory T (Treg) cells in maintaining peripheral tolerance and autoimmunity. The number and functional capabilities have been reported to be low in several diseases including RA, which affects the immune regulatory action of Treg cells. Proinflammatory cytokines such as tumor necrosis factor α (TNF-α), are important in RA pathogenesis, but the influence on Treg cells is poorly understood. Methods: In the present study, the messenger RNA (mRNA) expressions of FOXP3 and TNF-α in a group of patients with RA (N=23) and a healthy control group (N=17) were studied in peripheral blood mononuclear cells (PBMCs). PBMCs were chosen as they are practical samples in which changes caused by disease or therapy can be conveniently monitored. Results: Expression of FOXP3 was lower (P<0.0001, 0.76 folds) and TNF-α gene expression was higher (P<0.0001, 2.28 folds) in RA patients when compared with the healthy control group. However, a statistically significant correlation could not be established between the FOXP3 and disease activity, but relative mRNA expression of FOXP3 and TNF-α showed a statistically significant correlation (P<0.0283) in RA patients when compared with the healthy control group. Conclusions: The results suggested that decreased expression of FOXP3 gene and increased level of TNF-α expression in the presence of rheumatoid factor antibodies (RF) may impair the activity of Treg cells with higher TNF-α levels when compared with patients who were negative for RF. Level of Evidence: Level II.