Comparison of Tumor Necrosis Factor Alpha and Insulin Resistance in Obeseversus Non-obese Type 2 Diabetic Patients
AbstractType 2 diabetes mellitus (T2DM) and insulin resistance (IR) are linked to each other. Obesity and T2DM are states of low-grade chronic inflammation, which result in increased levels of inflammatory markers such as C-reactive protein (CRP), interleukins 6 (1L-6) and tumor necrosis factor alpha (TNF-α). Relation of TNF-α with obesity induced IR and T2DM is unclear as results obtained from different studies are very controversial. Objective: This study was designed to compare TNF-α levels and insulin resistance in obese and non-obese type 2 diabetics. Methodology: A cross sectional comparative study was conducted in diabetic clinic of Mayo Hospital, Lahore. We determined and compared TNF-α levels and insulin resistance in 90 subjects where there were 50 obese patients with T2DM and 40 were non-obese Type 2 diabetic patients. TNF-α and serum insulin levels were determined using ELISA. Insulin resistance was calculated using HOMA-IR. Comparison between groups was performed using independent sample t-test. The P value ≤ 0.05 was considered statistically significant. Results: Mean HOMA-IR and TNF-α values were significantly (p-value <0.01) higher in obese diabetics (17.13+8.77) and (10.96+4.69), respectively when compared to non-obese Type 2 diabetic patients (3.40+5.05) and (3.49+2.36) respectively. Mean HOMA-IR in males was 6.52+7.03 and in females was 12.85+10.54 (p-value 0.006). Conclusion: Increased inflammation in obese diabetics explains the role of tumor necrosis factor alpha in insulin resistance induced by obesity. Weight reduction in obese individuals will help in reducing TNF-α levels and to improve insulin sensitivity in T2DM.
This work is licensed under a Creative Commons Attribution 4.0 International License.
This is an open-access journal and all the published articles / items are distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.