An examination of β-cell function measures and their potential use for estimating β-cell mass

A characteristic and dominant feature of type 2 diabetes is a reduction in β-cell function that is associated with a decrease in β-cell volume. A decline in the first-phase insulin response following intravenous glucose administration can be demonstrated as the fasting glucose concentration increases. This response is completely absent before the glucose threshold that defines diabetes has been reached and at a time when β-cells are clearly still present, implying that a functional β-cell lesion has to exist independent of β-cell loss. Surgical or chemical reductions of up to 65% of β-cell volume demonstrate that functional adaptation of the normal β-cell prevents a rise in fasting glucose or reduction in first-phase insulin response. However, the ability of glucose to potentiate the β-cell’s response to non-glucose secretagogues is reduced and is more closely associated with the reduction in β-cell volume. The future, in terms of prevention and treatment of type 2 diabetes, lies in the ability to prevent and revert both β-cell loss and dysfunction. However, until β-cell volume can be quantified reliably and non-invasively, we will need to rely on the ability of glucose to potentiate insulin release as the best surrogate estimate of the number of β-cells.