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Updated: Mar 31, 2026

Multidisciplinary Approach to Obesity Management: A Case Report
Published on: May 30, 2025
Treatment of prediabetes
Mustafa Kanat1, Ralph A DeFronzo1, Muhammad A Abdul-Ghani1
1Mustafa Kanat, Division of Diabetes, Department of Internal Medicine, Istanbul Medipol University, 34214 Istanbul, Turkey.
Preventing type 2 diabetes involves managing impaired glucose tolerance (IGT). Lifestyle changes and medications can improve insulin sensitivity and preserve beta-cell function, slowing progression from IGT to type 2 diabetes mellitus.
Area of Science:
- Endocrinology
- Metabolic Disorders
- Diabetes Research
Background:
- Impaired glucose tolerance (IGT) is a transitional state between normal glucose tolerance (NGT) and type 2 diabetes mellitus (type 2 DM).
- Beta-cell dysfunction and insulin resistance are key defects in type 2 DM and are also present in IGT, contributing to disease progression.
- Interventions targeting insulin sensitivity and beta-cell function are crucial for managing IGT and preventing type 2 DM.
Purpose of the Study:
- To review lifestyle modifications and pharmacologic agents for preventing the conversion of IGT to type 2 DM.
- To discuss strategies for improving insulin sensitivity and preserving beta-cell function in prediabetic individuals.
Main Methods:
- This review discusses existing literature on lifestyle modifications (e.g., weight loss) and pharmacologic treatments for IGT.
- Evidence regarding the impact of these interventions on insulin sensitivity and beta-cell function is examined.
Main Results:
- Weight loss improves insulin sensitivity and preserves beta-cell function, showing a potential to inhibit IGT progression.
- Pharmacotherapy offers an alternative approach to enhance insulin sensitivity and maintain beta-cell function.
Conclusions:
- Both lifestyle modifications and pharmacologic agents represent viable strategies to limit the progression from IGT to type 2 DM.
- Effective management of IGT is essential for diabetes prevention and requires addressing underlying metabolic defects.
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