Abstract
BACKGROUND: In the development and progression of type 2 diabetes mellitus, β-cell dysfunction occurs after insulin resistance. Despite poor glycaemic control, there is a practice of increasing the dose of oral anti-diabetics or adding more drugs to the regimen due to the common perception that low endogenous insulin secretion is related to type 1 diabetes mellitus only and patient's poor compliance to injectables. Keeping this perspective in mind, this study was conducted to assess the prevalence of beta cell dysfunction by low serum C-peptide levels and its correlation with poor glycaemic control. MATERIALS AND METHODS: A total of 134 patients with type 2 diabetes mellitus for more than 10 years on oral anti-diabetic drugs fulfilling our eligibility criteria were enrolled in our study. Blood samples for fasting blood sugar and fasting C-peptide level were taken before breakfast and uptake of anti-diabetic drugs. Correlation analysis was performed to evaluate the relationship between fasting C-peptide and glycaemic control with respect to glycated haemoglobin (HbA1c). RESULTS: Of the patients, 19.40% had insufficient beta cell reserve serum levels (C-peptide < 0.5 ng/ml), of which most of the patients (14/26 = 53.85%) had poor glycaemic control (HbA1c < 8.0%). Overall, there was a significant correlation between poor glycaemic control with respect to HbA1c and low serum C-peptide levels (p < 0.05). We found a significant association of beta cell dysfunction (low fasting C-peptide level) with the use of insulin secretagogue. The proportion of patients with C-peptide levels less than 0.5 ng/ml was lower in patients using sodium-glucose cotransporter-2 (SGLT-2) inhibitors as compared to insulin secretagogue. CONCLUSION: SGLT-2 inhibitors should be preferred over other anti-diabetic drugs as an add-on to existing metformin therapy. Insulin requirement must be assessed in patients who have long-term type 2 diabetes mellitus.