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Clinical Diabetes 25:131-134, 2007
DOI: 10.2337/diaclin.25.4.131
© 2007 by the American Diabetes Association
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Diabetes Foundation

Diabetes Treatment, Part 2: Oral Agents for Glycemic Management

Michael J. Fowler, MD

The first 300 words of the full text of this article appear below.


    Introduction
 
The epidemic of type 2 diabetes in the United States and the rest of the world continues to grow rapidly; as many as 20 million people in the United States may have the disease.1 The vast majority of people with diabetes have type 2 diabetes, caused by a relative insulin deficiency superimposed on a background of insulin resistance.2 Most patients begin treatment with diet and exercise or incorporate them into their treatment regimen, but, unfortunately, most patients are unsuccessful in controlling type 2 diabetes through lifestyle modification alone and require pharmacotherapy.

For several reasons, oral agents are typically the first medications used in the treatment of type 2 diabetes. Because of their wide range of efficacy, safety, and mechanisms of action, it is important for clinicians to gain a broad understanding of each class of oral agents to optimize diabetes control. This article reviews the major classes of oral agents used to treat type 2 diabetes, with an emphasis on the benefits and risks of each class. It is important to note that because type 1 diabetes results from an absolute deficiency of pancreatic β-cells, most oral agents are not indicated in the treatment of patients with type 1 diabetes. Oral agents are also largely not tested or approved for use in pregnancy.


    Metformin
 
Metformin is the sole member of the biguanide class of medications in the United States. It replaced another biguanide, fenformin, which was removed from the market because of a propensity for lactic acidosis in 1975.3,4 Available in short-acting and sustained-release formulations, it is one of the oldest, and indeed one of the safest, medications used in the treatment of type 2 diabetes.

Metformin exerts its effects primarily by decreasing hepatic glucose output and has a comparatively lesser effect increasing insulin sensitivity. Isotope studies suggest hepatic glucose . . . [Full Text of this Article]


    Sulfonylureas
 

    Glinides
 

    Thiazolidinediones
 

    {alpha}-Glucosidase Inhibitors
 

    DPP-IV Inhibitors
 

    Conclusion
 

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Copyright © 2007 by the American Diabetes Association.