Progressive decline of β-cell function is a hallmark of disease progression
in type 2 diabetes mellitus (T2DM). β-cell dysfunction may precede
the onset of T2DM by several years.1 Studies show a decline of
approximately 50% in β-cell function at T2DM diagnosis, with a further
drop of 4% expected each year.2
Landmark longitudinal studies such as the Veterans Affairs Diabetes
Trial (VADT) and the United Kingdom Prospective Diabetes Study
(UKPDS) have demonstrated the importance of β-cell function in
maintaining glycaemic control and as an indicator of disease status.3,4
A progressive decline in C-peptide levels from diagnosis until 18 years
of diabetes duration was observed in the VADT, while in the UKPDS,
homeostatic model assessment of β-cell function (HOMA-B) was 50%
at time of diagnosis and 28% after 6 years. Early intervention is
deemed as a potential approach in reducing the risk of complications
due to hyperglycaemia, and β-cell status may play a crucial role in clinical decision making to facilitate appropriate and timely treatment
initiation
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