Glycaemic Variability and Pancreatic ß-cell Dysfunction
2012
The importance of glycaemic variability (GV) as a factor in the pathophysiology of cellular dysfunction and
late diabetes complications is currently a matter of debate. However, there is mounting evidence from in vivo and in vitro
studies that GV has adverse effects on the cascade of physiological processes that result in chronic s-cell dysfunctions.
Glucose fluctuations more than sustained chronic hyperglycaemia can induce excessive formation of reactive oxygen
(ROS) and reactive nitrogen species (RNS), ultimately leading to apoptosis related to oxidative stress. The insulinsecreting
s-cells are particularly susceptible to damage imposed by oxidative stress. Evidence from experiments, using
isolated pancreatic islets or s-cell lines, has linked intermittent high glucose, which mimicks GV under diabetic conditions,
to significant impairment of s-cell function. Several clinical studies reported a close association between GV and scell
dysfunction, although the deleterious effects are difficult to demonstrate. Notwithstanding, early therapeutic interventions
in patients with type 1 as well as type 2 diabetes, using different strategies of optimising glycaemic control, have
shown that favourable outcomes on recovery and maintenance of s-cell function correlated with reduction of GV. The
purpose of the present review is to discuss the detrimental effects of GV and associations with s-cell function as well as
upcoming therapeutic strategies directed towards minimising glucose excursions, improving s-cell recovery and preventing
progressive s-cell loss. Measuring GV has importance for management of diabetes, because it is the only one component
of the dysglycaemia that reflects the degree of dysregulation of glucose homeostasis.
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