Adams JD, Man CD, Laurenti MC, et al. - Given that abnormal glucagon concentrations are a characteristic of prediabetes but it is doubtful whether α-cell dysfunction contributes to a longitudinal decline in β-cell function, researchers conducted this longitudinal study to determine if a decline in β-cell function is correlated with higher nadir glucagon in the postprandial period or with higher fasting glucagon. For this investigation, 73 non-diabetic individuals were analyzed on two occasions 6.6 ± 0.3 years apart using a 2-h, 7-sample oral glucose tolerance test. Defects in α-cell function, express as elevated fasting glucagon, are related to a subsequent decline in β-cell function. It remains to be ascertained whether the abnormal α-cell function in the pathogenesis of T2D directly contributes to loss of β-cell secretory capacity.