Abstract

Objectives:We aimed to determine the effect of short-term intensive insulin therapy (SIIT) on long-term glycemic control in newly-diagnosed Type-2 diabetes mellitus (nT2DM) patients.Methods:In this retrospectively study conducted at Sakarya University Medical Faculty Training and Research Hospital Outpatient Clinic between 2016 and 2019, 65 nT2DM patients were enrolled soon after their SIIT was initiated and were followed for at least a year. Intensive insulin treatment was discontinued after three or 12 months in a total of 65 (23–73-year-old) patients who had been newly diagnosed with T2DM. Intensive insulin therapy was discontinued when glycemic control and the target Glycated Hemoglobin (HbA1c) level had been attained, after which oral anti-diabetic drug (OAD), long-term insulin, and diet therapies were pursued.Results:There was a significant decrease in mean HbA1c from 11.25±1.96% to 6.67±1.07%. Fasting plasma glucose (FPG) was found to be an independent predictor of whether intensive insulin therapy could be discontinued after three months in a model that included FPG, HbA1c, and body mass index measured at baseline. Patients with FPG>13.8 mmol/L were 7.6 times more likely to require intensive insulin therapy beyond three months. There were significant decreases in HbA1c and low-density lipoprotein-cholesterol concentration, but no change in C-peptide between baseline and 3 months of therapy.Conclusion:These results demonstrate that in nT2DM patients, intensive insulin therapy could be effective on long-term glycemic control and high FPG prior to three months of SIIT may predict poor long-term glycemic control.

Highlights

  • Type-2 diabetes mellitus (T2DM) is caused by an insulin deficiency that develops following chronic progressive beta-cell dysfunction

  • fasting plasma glucose (FPG) 4.4-7.2 mmol and PPG 10 or

  • We found that FPG, PPG, HbA1c, LDLcholesterol, and ALT were significantly lower after 3 and 12 months than at baseline

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Summary

Introduction

Type-2 diabetes mellitus (T2DM) is caused by an insulin deficiency that develops following chronic progressive beta-cell dysfunction. An increase in circulating C-peptide concentration during the early stage of insulin therapy is the most important indicator of improvement in the endogenous beta-cell reserve.[3] there have been few studies in which control was shown to be achieved using shortterm intensive insulin therapy (SIIT) from as early as the first three months following diagnosis.[4,5,6]. A systematic review and meta-analysis recently demonstrated that 2–8 weeks of early, intensive insulin therapy can induce glycemic control, and after its discontinuation, patients can subsequently. We aimed to investigate the effects of SIIT on longterm glycemic control in newly diagnosed T2DM patients in this retrospective study

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