The significance of tumor necrosis factor-α in newly diagnosed type 2 diabetic patients by transient intensive insulin treatment

Abstract 

This study was performed to investigate whether transient intensive insulin therapy with an insulin pump (TIIT) can decrease serum tumor necrosis factor-α (TNF-α) and explore whether the decrease of serum TNF-α has correlation with the improvement of islet β-Cell function and the decrease of insulin resistance. Thirty healthy volunteers served as control subjects. One hundred and thirty-eight newly diagnosed type 2 diabetic patients had been treated with TIIT for 2 weeks. TNF-α, free fatty acids (FFAs), glucose, and insulin (INS) had been measured before and after TIIT, respectively. Homeostasis model assessment (HOMA) was used to estimate insulin resistance (HOMA-IR) and islet β-Cell function (HOMA-β). TNF-α was significantly increased in diabetes. After TIIT, TNF-α, fasting blood glucose, FFAs, and HOMA-IR were significantly decreased. HOMA-β and the areas under the curves of INS were significantly increased during intravenous glucose tolerance tests. TNF-α had not only significant negative correlation with the changes of insulin secretion, but also significant positive correlation with the changes of HOMA-IR after adjustment of blood glucose. Partial correlation analyses demonstrated that there was an indepenent relationship between TNF-α and HOMA-IR and HOMA-β. Our study confirms that TIIT can effectively decrease serum TNF-α in type 2 diabetes. It is inferred that the decrease of serum TNF-α might be involved in the improvement of β-Cell function and the decrease of insulin resistance by TIIT.

Abbreviations: AUC, the areas under the curves, FFAs, free fatty acids, FPG, fasting plasma glucose, HOMA, homeostasis model assessment, INS, insulin, IVGTT, intravenous glucose tolerance tests, PPG, postprandial 2h plasma glucose, TIIT, transient intensive insulin therapy with an insulin pump, TNF-α, tumor necrosis factor-α

Keywords: Diabetes mellitus, Non-insulin-dependent, β-Cell function, Insulin resistance, Tumor necrosis factor-α