Predicting Diabetes Using Measures of β-Cell Function

  1. Alan R. Zinsmeister2
  1. 1Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic, Rochester, Minnesota
  2. 2Division of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, Minnesota
  1. Corresponding author: Adrian Vella, vella.adrian{at}mayo.edu.

Type 2 diabetes causes significant morbidity and mortality, making diabetes prevention a worthwhile goal. Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) have high rates of progression to type 2 diabetes. In Olmsted County, MN, 40% of people with a fasting glucose ≥110 mg/dL progressed to overt diabetes within a 10-year period, compared with 5% of those with fasting glucose <95 mg/dL (1). What explains why 60% of people with a fasting glucose ≥110 mg/dL did not progress to diabetes? One answer is that IFG encompasses individuals with differing glucose tolerance, some of whom might have normal glucose tolerance (NGT) whereas others have IGT (2). This is supported by the observation that postchallenge glucose concentrations are a better predictor of diabetes risk than fasting concentrations (3).

Maintenance of glucose tolerance is largely dependent on insulin secretion and insulin action—the ability of insulin to stimulate glucose uptake and suppress glucose release. Other parameters that may contribute to defects in glucose tolerance include hepatic insulin clearance, which determines systemic insulin bioavailability (4).

In this issue of Diabetes, Giannini et al. (5) examined the progression of glucose intolerance in obese adolescents, seeking to determine whether defects in insulin secretion and action are apparent within the normal range of glucose tolerance (based on 2-h glucose values). …

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