Abstract
Increased risk of cerebrovascular accident in diabetes cannot be fully explained by
traditional risk factors. Epidemiological studies show that postprandial hyperglycemia
is strongly associated with cerebrovascular events and cerebrovascular-associated
mortality. Postprandial hyperglycemia contributes to vascular damage by several mechanisms
such as endothelial dysfunction, arthrosclerosis, oxidative stress, inflammation,
and hypercoagulability. Hyperglycemia has deleterious effects on the vascular endothelium
and leads to the development of cerebrovascular disease. Thus, an important strategy
to reduce cerebrovascular risk in patients with diabetes is to reduce postprandial
hyperglycemia. Glucagon-like peptide-1 receptor agonists, dipeptidyl peptidase-4 inhibitors,
and α-glucosidase inhibitors predominantly reduce postprandial plasma glucose levels.
Among all of these, α-glucosidase inhibitors reduces postprandial hyperglycemia by
delaying carbohydrate absorption from the intestine and this mechanism provides glycemic
control without exacerbating coexisting cerebrovascular risk factors. Good glycemic
control is proven to reduce the risk of cardiovascular complications, but equivalent
evidence for cerebrovascular risk reduction is lacking. This review examines the evidences
that postprandial hyperglycemia plays a major role in vascular damage, along with
the complex interplay between hyperglycemia and coexisting risk factors. Furthermore,
the mechanism by which α-glucosidase inhibitors may prevent this vascular damage as
well as risk of hypoglycemia with α-glucosidase inhibitors are examined. Thus, this
review suggests that α-glucosidase inhibitors are useful in reducing the risk of cerebrovascular
events in patients with diabetes.
Key words
α-glucosidase inhibitors - cerebrovascular accident - diabetes - hyperglycemia - vascular
damage
