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Unmet needs among patients with type 2 diabetes and secondary failure to oral anti-diabetic agents

D Pitocco1, D Valle, A Rossi

  • 1Institute of Medical Pathology, Catholic University of Sacred Heart, 00168 Rome, Italy. dariopitocco@virgilio.it

Journal of Endocrinological Investigation
|May 14, 2008
PubMed

Insights

Secondary failure in Type 2 diabetes occurs when oral antidiabetic drugs (OAD) become less effective due to declining beta-cell function. New therapies like incretin mimetics show promise in improving glycemic control and beta-cell function.

Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Pharmacology

Background:

  • Secondary failure, a decline in glucose control in Type 2 diabetes patients on oral antidiabetic drugs (OAD), is primarily caused by progressive beta-cell dysfunction and reduced insulin secretion.
  • Hyperglycemia resulting from secondary failure is a key factor in microvascular and macrovascular complications.
  • Lowering target glycosylated hemoglobin (HbA1c) levels necessitates tighter glycemic control, making secondary failure to OAD more frequent and almost unavoidable.

Purpose of the Study:

  • To review current treatment strategies for secondary failure in Type 2 diabetes.
  • To identify barriers to achieving and maintaining glycemic control.
  • To examine emerging therapies, particularly incretin mimetics and thiazolidinediones, for patients failing OAD, focusing on their impact on beta-cell function.

Main Methods:

  • Review of current literature on Type 2 diabetes secondary failure.
  • Analysis of therapeutic strategies including OAD, incretin mimetics (exenatide, liraglutide), and thiazolidinediones.
  • Focus on mechanisms of action, particularly effects on beta-cell function and insulin resistance.

Main Results:

  • Incretin mimetics demonstrate a lowering effect on HbA1c by improving beta-cell function, accompanied by significant weight loss.
  • Thiazolidinediones primarily address insulin resistance.
  • Co-administration of OAD with incretin mimetics is a key emerging strategy.

Conclusions:

  • Incretin mimetics offer a promising therapeutic option for secondary failure in Type 2 diabetes by enhancing beta-cell function and promoting weight loss.
  • While current evidence suggests improved outcomes, further long-term investigations are required to validate the efficacy of these novel therapies.
  • Addressing secondary failure is crucial for preventing diabetes-related complications and improving patient outcomes.

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