Preservation of β-cell function: The key to diabetes prevention

Ralph A Defronzo, Muhammad A Abdul-ghani

Research output: Contribution to journalArticle

138 Citations (Scopus)

Abstract

Context: The Centers for Disease Control and Prevention estimates that there are approximately 79,000,000 individuals in the United States with prediabetes [impaired glucose tolerance (IGT) and/or impaired fasting glucose] and that approximately 40-50% will progress to type 2 diabetes mellitus (T2DM) during their lifetime. Therefore, treatment of high-risk IGT individuals to prevent T2DM has important medical, economic, social, and human implications. Individuals in the upper tertile of IGT are maximally/near-maximally insulin resistant, have lost 70-80% of their β-cell function, and have approximately a 10% incidence of diabetic retinopathy. Therefore, preservation of the remaining 20-30% of β-cell function is critical to prevent future development of T2DM. Evidence Acquisition: We searched MEDLINE from 2000 to the present to identify placebo-controlled trials in which individuals with IGT received pharmacological therapy to prevent progression to diabetes. Evidence Synthesis: Lifestyle modification reduces IGT conversion to T2DM, but it is difficult to implement and maintain. Moreover, 40-50% of IGT subjects progress to T2DM despite weight loss. In contrast, pharmacological intervention with medications that reverse known pathophysiological abnormalities (β-cell dysfunction and insulin resistance) uniformly prevents IGT progression to T2DM. Thiazolidinediones reduce IGT conversion to diabetes by approximately 50-70%. Metformin in the U.S. Diabetes Prevention Program reduced the development of T2DM by 31% and has been recommended by the American Diabetes Association. Because glucagon-like peptide-1 analogs augment insulin secretion, preserve β-cell function, and promote weight loss, they may be efficacious in preventing IGT progression to T2DM. Conclusion: Pharmacological intervention with a variety of agents (thiazolidinediones, metformin, acarbose, glucagon-like peptide-1 analogs) consistently reduces the rate of conversion of IGT to T2DM.

Original languageEnglish (US)
Pages (from-to)2354-2366
Number of pages13
JournalJournal of Clinical Endocrinology and Metabolism
Volume96
Issue number8
DOIs
StatePublished - Aug 2011

Fingerprint

Glucose Intolerance
Medical problems
Type 2 Diabetes Mellitus
Glucose
Thiazolidinediones
Glucagon-Like Peptide 1
Metformin
Pharmacology
Insulin
Weight Loss
Acarbose
Medical Economics
Prediabetic State
Disease control
Diabetic Retinopathy
Centers for Disease Control and Prevention (U.S.)
MEDLINE
Insulin Resistance
Life Style
Fasting

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Endocrinology
  • Biochemistry, medical
  • Endocrinology, Diabetes and Metabolism

Cite this

Preservation of β-cell function : The key to diabetes prevention. / Defronzo, Ralph A; Abdul-ghani, Muhammad A.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 96, No. 8, 08.2011, p. 2354-2366.

Research output: Contribution to journalArticle

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abstract = "Context: The Centers for Disease Control and Prevention estimates that there are approximately 79,000,000 individuals in the United States with prediabetes [impaired glucose tolerance (IGT) and/or impaired fasting glucose] and that approximately 40-50{\%} will progress to type 2 diabetes mellitus (T2DM) during their lifetime. Therefore, treatment of high-risk IGT individuals to prevent T2DM has important medical, economic, social, and human implications. Individuals in the upper tertile of IGT are maximally/near-maximally insulin resistant, have lost 70-80{\%} of their β-cell function, and have approximately a 10{\%} incidence of diabetic retinopathy. Therefore, preservation of the remaining 20-30{\%} of β-cell function is critical to prevent future development of T2DM. Evidence Acquisition: We searched MEDLINE from 2000 to the present to identify placebo-controlled trials in which individuals with IGT received pharmacological therapy to prevent progression to diabetes. Evidence Synthesis: Lifestyle modification reduces IGT conversion to T2DM, but it is difficult to implement and maintain. Moreover, 40-50{\%} of IGT subjects progress to T2DM despite weight loss. In contrast, pharmacological intervention with medications that reverse known pathophysiological abnormalities (β-cell dysfunction and insulin resistance) uniformly prevents IGT progression to T2DM. Thiazolidinediones reduce IGT conversion to diabetes by approximately 50-70{\%}. Metformin in the U.S. Diabetes Prevention Program reduced the development of T2DM by 31{\%} and has been recommended by the American Diabetes Association. Because glucagon-like peptide-1 analogs augment insulin secretion, preserve β-cell function, and promote weight loss, they may be efficacious in preventing IGT progression to T2DM. Conclusion: Pharmacological intervention with a variety of agents (thiazolidinediones, metformin, acarbose, glucagon-like peptide-1 analogs) consistently reduces the rate of conversion of IGT to T2DM.",
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