Researchers’ understanding of
type 2 diabetes is being
reinvented before our eyes. Some time ago, there was a split among
diabetes
researchers about whether type 2 diabetes was driven by insufficient
insulin
production (beta-cell failure) or flawed insulin use in cells (insulin
resistance). Eventually a consensus was reached: beta-cell failure and
insulin
resistance both contribute to the progression of type 2 diabetes, and
both
abnormalities emerging, typically insulin resistance first. Researchers
then identified another problem
in type 2 diabetes: the over-production of glucose from the liver
(gluconeogensis), especially at inappropriate times such as after
meals. For some time, this palpable trio – insulin resistance,
beta-cell failure, and
increased gluconeogenesis – encompassed the mainstream understanding of
the
pathology of type 2 diabetes.
This trio is expanding before our eyes to encompass a wide
range of newly identified problems associated with type 2 diabetes. Suddenly researchers
are paying attention to abnormalities in gut hormones (incretins),
mitochondrial dysfunction and oxidative stress, inflammation, and even the
brain as drivers of type 2 diabetes. The newest member of the pack, abnormal
fat distribution, which has been standing on the sidelines since the earliest
descriptions of type 2 diabetes, suddenly finds itself in center field.