Objective: Type 2 diabetes is associated with defects in insulin secretion and insulin action. Hyperglycemia may aggravate these defects, a feature known as glucose toxicity. In such patients, exogenous insulin administration is often required to control blood glucose levels within a target range. Insulin is co-secreted with c-peptide, a biologically active amino acid polypeptide cleaved from the proinsulin molecule of pancreatic beta-cells. The aim of the present study to assess the effect of insulin therapy on early levels of c-peptide as a surrogate marker of beta-cell functions during hyperglycemia in patients with T2DM. We hypothesized that the magnitude of such hyperglycemia would be associated with the level of circulating c-peptide levels in patients with T2DM. Furthermore, we hypothesized that insulin administration would be associated with a greater increase in c-peptide levels in response to hyperglycemia which ultimately leads to preservation of beta cell function. Methods: Cross sectional observational study was done in TUTH. 24 patients who received early intensive insulin therapy at the time of diagnosis of type II DM were included in the study. Patients were treated with 2-3 week course of intensive insulin therapy that was followed by oral hypoglycemic drug. Changes in β-cell function by estimation of C-peptide and glycemic control during three weeks follow-up period was evaluated Results: Mean age of participants was 43+/-10.3 years. Male to female ratio was 3:1. BMI was 25+/-2.5 kg/㎡. Fasting glucose level after 3 weeeks fell from 12.9 ± 0.7 to 7.0 ± 0.1 mmol/L (p < 0.001). Insulin administration was independently associated with a greater increase in c-peptide (P = 0.04). Conclusion: These results demonstrate that in newly diagnosed type 2 diabetes with elevated fasting glucose levels, a short course of intensive insulin therapy can successfully improve beta cell function for prolonged good glycemic control.