Treatment of prediabetes
Progression of normal glucose tolerance (NGT) toovert diabetes is mediated by a transition state calledimpaired glucose tolerance (IGT). Beta cell dysfunctionand insulin resistance are the main defects in type 2diabetes mellitus (type 2 DM) and even normoglycemicIGT patients manifest these defects....
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Published in | World journal of diabetes Vol. 6; no. 12; pp. 1207 - 1222 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
United States
Baishideng Publishing Group Inc
25.09.2015
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Subjects | |
Online Access | Get full text |
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Summary: | Progression of normal glucose tolerance (NGT) toovert diabetes is mediated by a transition state calledimpaired glucose tolerance (IGT). Beta cell dysfunctionand insulin resistance are the main defects in type 2diabetes mellitus (type 2 DM) and even normoglycemicIGT patients manifest these defects. Beta cell dysfunctionand insulin resistance also contribute to the progressionof IGT to type 2 DM. Improving insulin sensitivity and/orpreserving functions of beta-cells can be a rational wayto normalize the GT and to control transition of IGT totype 2 DM. Loosing weight, for example, improves wholebody insulin sensitivity and preserves beta-cell functionand its inhibitory effect on progression of IGT to type 2DM had been proven. But interventions aiming weightloss usually not applicable in real life. Pharmacotherapyis another option to gain better insulin sensitivity andto maintain beta-cell function. In this review, twopotential treatment options (lifestyle modification andpharmacologic agents) that limits the IGT-type 2 DMconversion in prediabetic subjects are discussed. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 Correspondence to: Dr. Mustafa Kanat, MD, Division of Diabetes, Department of Internal Medicine, Istanbul Medipol University, TEM Avrupa Otoyolu Göztepe Çıkışı No: 1, Bağcılar, 34214 Istanbul, Turkey. mustafa.kanat@gmail.com Telephone: +90-542-3131400 Author contributions: All authors contributed to this manuscript. |
ISSN: | 1948-9358 1948-9358 |
DOI: | 10.4239/wjd.v6.i12.1207 |