Metabolic syndrome: the dysmetabolic state of dysfunctional adipose tissue and insulin resistance

Abstract

The current world epidemic of obesity represents a tremendous medical and public health challenge. A major consequence of obesity has been a rapid acceleration in the prevalence of type 2 diabetes;1 however, it is now recognized that even before the development of diabetes, many individuals have the constellation of athero-thrombotic inflammatory abnormalities characteristic of type 2 diabetes.2 Thus, the cluster of metabolic abnormalities is not the consequence of the hyperglycaemic state of type 2 diabetes but is rather pathophysiologically related to insulin resistance, the most prevalent form of insulin resistance being present in individuals with excess visceral as well as ectopic fat.3 Thus, even in the absence of hyperglycaemia, abdominally obese patients with an excess of visceral and ectopic fat deposition are likely to have the clustering of risk factors associated with insulin resistance. In this regard, the pivotal role of insulin resistance in the pathophysiology of the cluster of risk factors was first reported by Reaven4 and designated syndrome X. Since his seminal paper, numerous groups have utilized the term insulin resistance syndrome in the description of this cluster of athero-thrombotic inflammatory abnormalities.5,6 In 2001, the guidelines developed by the National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATP III) committee considered abdominal obesity as central in the pathophysiological development of the insulin resistance syndrome.7 Since the measurement of insulin resistance was not practical in the context of primary care clinical practice, the guidelines provided clinicians with simple diagnostic criteria, including waist circumference, triglycerides, high-density …