814-P: Intensive Insulin Therapy within One Week Can Improve ß-Cell Function in T2D Patients Free

Objective: Short-term intensive insulin therapy (IIT), usually over 2 weeks, can improve β-cell function in T2D. However, whether shorter duration of IIT could also have impact on β-cell function remained unclear. This study was thus designed to explore this question.

Methods: One hundred and ninety-two T2D patients who received continuous subcutaneous insulin infusion within 1 week and underwent comprehensive evaluation of β-cell function before and after IIT were included. β-cell function indices including HOMA-β, insulinogenic index, disposition index (DI), fasting and postprandial C-peptide index (CPI), AUC of insulin and C-peptide were adopted. In a subset patients underwent CGM, the correlation of glucose variability and β-cell function were analyzed.

Results: The patients were 56.2±13.7 (mean±SD) years old, with diabetic duration of 6.0 (12.1) [median (interquartile)] years, HbA1c of 9.3±2.0%. After 3-7 days (median: 5 days) of IIT, insulinogenic index [3.6 (5.3) mU/mmol vs. 2.9 (4.4) mU/mmol, p=0.005], DI [358.3 (398.5) vs. 233.3 (275.5), p<0.001], fasting CPI [1.2 (0.8) nmol/mmol vs. 1.0 (0.8) nmol/mmol, p<0.001], postprandial CPI [1.8 (1.5) nmol/mmol vs. 1.4 (1.2) nmol/mmol, p<0.001] and AUC of C-peptide [113.0 (67.1) nmol∙min/L vs. 103.7 (55.9) nmol∙min/L, p=0.002] were significantly improved compared with baseline. Among these patients, 45 subjects underwent CGM. It was found that changes in DI from baseline (ΔDI) were negatively correlated with TAR (r=-0.417, P=0.004), standard deviation (r=-0.366, P=0.013), MAGE (r=-0.295, P=0.049), glucose coefficient of variation (r=-0.321, P=0.031) and positively correlated with TIR (r=0.359, P=0.004). Multiple linear regression revealed that duration of IIT (β=0.453, P=0.009) and TIR (β=0.527, P=0.006) were independent factors of ΔDI.

Conclusions: IIT within 1 week can also improved β-cell function in T2D patients. Duration of IIT and TIR could be the independent factors responsible for the improvement of β-cell function.