Abstract

β-Cell function should be expressed as insulin secretion in relation to the prevailing and changing glucose concentration and interpreted in light of prevailing insulin resistance. Characterizing alterations in β-cell function in individuals with impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) (collectively termed “prediabetes”) has been a hotly pursued topic among clinical investigators over the past several years. Because IFG and IGT are both associated with elevated risk of progression to overt type 2 diabetes and cardiovascular events (1–3), it is important to understand the specific defects in β-cell function that occur in these settings. Such knowledge could translate into targeted therapeutic interventions that could potentially delay or halt the progression of IFG/IGT to frank diabetes. In this issue of Diabetes , Abdul-Ghani and colleagues (4) attempt to characterize changes in β-cell function in a group of middle-aged, obese, predominantly female Mexican Americans with and without prediabetes using the frequently sampled oral glucose tolerance test (OGTT) and in subgroups using the hyperglycemic clamp technique. Applying published models and methods (5), the authors identified distinct defects in β-cell function in response to oral/intravenous glucose load in individuals with IFG and …

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