The
metabolic syndrome is strongly associated with
insulin resistance and has been recognized as a cluster of risk factors for
cardiovascular diseases such as
visceral obesity,
hypertension, diabetes, and atherogenic
dyslipidemia. Recently,
insulin resistance in the absence of overt diabetes or the
metabolic syndrome itself has been associated with endothelial dysfunction, one of the initial steps in the process of
atherosclerosis.
Postprandial hyperglycemia, one of the characteristic features of
insulin resistance, induces oxidative stress generation and elicits vascular
inflammation and platelet activation, thus being involved in the pathogenesis of
atherosclerosis. A recent multicenter, placebo-controlled randomized trial, STOP-
NIDDM trial, revealed that
acarbose (
Glucobay R), an
alpha-glucosidase inhibitor, improved
postprandial hyperglycemia and subsequently reduced the risk of development of
type 2 diabetes in patients with
impaired glucose tolerance (IGT). In this study,
acarbose treatment was also found to slow the progression of intima-media thickness of the carotid arteries, a
surrogate marker for
atherosclerosis, and to reduce the incidence of
cardiovascular diseases and newly diagnosed
hypertension in subjects with IGT.
Acarbose significantly reduced body mass index and waist circumference in these patients over 3 years. Furthermore, a meta-analysis of seven long-term studies has also shown that intervention with
acarbose prevents
myocardial infarction and
cardiovascular diseases in type 2 diabetic patients. In this analysis,
glycemic control,
triglyceride levels,
body weight and systolic blood pressure was also significantly improved during
acarbose treatment. These observations suggest that prevention of
postprandial hyperglycemia by
acarbose may be a promising therapeutic strategy for reducing the increased risk for diabetes,
hypertension,
dyslipidemia,
obesity, and
cardiovascular diseases in patients with the
metabolic syndrome.
Acarbose improves
postprandial hyperglycemia by delaying the release of
glucose from complex
carbohydrates in the absence of an increase in insulin secretion. Therefore, we would like to hypothesize here that this improvement in
glucose metabolism could be associated with amelioration in
insulin sensitivity, thus explaining the above-mentioned beneficial cardiometabolic actions of
acarbose. Large clinical trials will provide us with more definite information whether
acarbose treatment can improve
insulin sensitivity and resultantly reduce the risk of diabetes,
hypertension and
cardiovascular diseases in patients with the
metabolic syndrome.