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Choice of early treatment regimen and impact on β-cell preservation in type 2 diabetes


  • S. Mudaliar

    Corresponding author
    1. Clinical Professor of Medicine, University of California, San Diego, CA, USA
    • Center for Metabolic Research, VA San Diego Healthcare System, San Diego, CA, USA
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  • Disclosures
    S. Mudaliar is a consultant for Bristol-Myers Squibb, AstraZeneca, Boehringer Ingleheim, and Roche Pharmaceuticals. He has served on the speaker's bureau for Bristol-Myers Squibb and AstraZeneca.

Correspondence to:

Sunder Mudaliar,

Section of Diabetes/Metabolism, VA San Diego Healthcare System, 3350 La Jolla Village Dr., San Diego, CA 92161, USA

Tel.: +1 858 642 3152

Fax: +1 858 642 6242



The progressive deterioration of glycaemic control in individuals with type 2 diabetes mellitus (T2DM) results from insulin resistance combined with the ongoing loss of β-cell function. Although it had been suggested that most β-cell dysfunction occurs after the development of T2DM, studies have documented a substantial early loss of β-cell function, particularly during the prediabetic state. In patients diagnosed with T2DM, β-cell function continues to decline despite treatment with commonly prescribed antihyperglycaemic medications, and ultimately exogenous insulin administration is required to maintain optimal glycaemic control. Thus, interventions to address the early decline in β-cell function could potentially alter the course of T2DM, preventing or delaying its onset and decreasing the incidence of complications. Original research and review articles on this topic were identified in a PubMed search from January 2000 through August 2012. Data from prospective studies and clinical trials suggest that lifestyle modifications and certain antihyperglycaemic medications, including thiazolidinediones (TZDs), glucagon-like peptide-1 (GLP-1) agonists, dipeptidyl peptidase-4 (DPP-4) inhibitors and insulin, may preserve or enhance β-cell function. The implication of current data is that early initiation of lifestyle modifications and antihyperglycaemic agents that preserve β-cell function might reverse or delay progression to T2DM in those with prediabetes. Moreover, improved β-cell function may confer more durable glucose control and perhaps reduce/delay the incidence of diabetic complications. Long-term studies are needed to validate this hypothesis.