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Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Sep 25, 2015; 6(12): 1207-1222
Published online Sep 25, 2015. doi: 10.4239/wjd.v6.i12.1207
Treatment of prediabetes
Mustafa Kanat, Ralph A DeFronzo, Muhammad A Abdul-Ghani
Mustafa Kanat, Division of Diabetes, Department of Internal Medicine, Istanbul Medipol University, 34214 Istanbul, Turkey
Ralph A DeFronzo, Muhammad A Abdul-Ghani, Diabetes Division, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, United States
Author contributions: All authors contributed to this manuscript.
Conflict-of-interest statement: Ralph A DeFronzo is a member of the Bristol-Myers Squibb, Janssen, Amylin, Takeda, Novo Nordisk, and Lexicon advisory boards; has received grants from Takeda, Amylin, and Bristol-Myers Squibb; and is a member of the following speakers bureaus: Bristol-Myers Squibb, Novo Nordisk, Janssen, and Takeda. No other potential conflicts of interest relevant to this article were reported.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
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
Received: December 23, 2014
Peer-review started: December 26, 2014
First decision: February 10, 2015
Revised: August 15, 2015
Accepted: September 7, 2015
Article in press: September 8, 2015
Published online: September 25, 2015
Processing time: 293 Days and 18.8 Hours
Core Tip

Core tip: Behavioral changes (dieting plus exercising) are effective in preventing impaired glucose tolerance (GT)-type 2 diabetes mellitus (type 2 DM) conversion as well as impaired fasting glucose (FG) - type 2 DM conversion but loosing weight is hard and also difficult to maintain. Pharmacological interventions (plus dieting and exercising) improving and preserving beta-cell function and enhancing insulin sensitivity may be suitable choices for high-risk IGT patients. Troglitazone in Prevention of Diabetes Study, Pioglitazone in Prevention of Diabetes Study, Diabetes Reduction Assessment with ramipril and rosiglitazone Medication Trial, Actos Now for the prevention of diabetes study and Diabetes Prevention Program have proven that thiazolidinediones obviously prevent the development of type 2 DM in IGT subjects as well as IFG subjects. In Diabetes Prevention Program and Indian Diabetes Prevention Program, metformin slowed down the progression of IGT to type 2 DM, and eventually American Diabetes Association Consensus Conference Statement proposed metformin usage in high-risk IGT individuals. However, the efficacy of pioglitazone and rosiglitazone efficacy in preventing IGT progression to type 2 DM nearly doubles metformin’s efficacy (31% vs 72% and 62%, respectively). Rosiglitazone (low dose = 2 mg/d) together with metformin (850 mg/d) was proven to slow down IGT progression to type 2 DM as well as being more tolerable.