DOES INSULIN-RESISTANCE UNITE THE SEPARATE COMPONENTS OF THE INSULIN-RESISTANCE SYNDROME - EVIDENCE FROM THE MIAMI COMMUNITY-HEALTH STUDY

Citation
Rp. Donahue et al., DOES INSULIN-RESISTANCE UNITE THE SEPARATE COMPONENTS OF THE INSULIN-RESISTANCE SYNDROME - EVIDENCE FROM THE MIAMI COMMUNITY-HEALTH STUDY, Arteriosclerosis, thrombosis, and vascular biology, 17(11), 1997, pp. 2413-2417
Citations number
35
ISSN journal
10795642
Volume
17
Issue
11
Year of publication
1997
Pages
2413 - 2417
Database
ISI
SICI code
1079-5642(1997)17:11<2413:DIUTSC>2.0.ZU;2-R
Abstract
A number of coronary heart disease risk factors have been identified t hat often cluster together to increase the risk of macrovascular disea se. This cluster is referred to as the insulin resistance syndrome, an d the risk factors commonly include dyslipidemia, elevated blood press ure, an android pattern of body fat distribution, and glucose intolera nce. Whether hyperinsulinemia or insulin resistance per se provides a common pathway for these metabolic abnormalities is unclear. The autho rs studied 50 nondiabetic persons who had completed a euglycemic hyper insulinemic clamp protocol in addition to a 75-g oral glucose toleranc e test and other measures of the coronary risk profile. Using principa l-component analysis, we reduced nine coronary risk factors to two unc orrelated factors that explained 54.5% of the variance; Factor 1 consi sted of positive loadings for uric acid, systolic and diastolic blood pressure, triglyceride concentration, and waist girth and negative loa dings for HDL cholesterol and the rate of insulin-mediated glucose dis posal (M, in milligrams per kilogram of body weight per minute). M als o loaded on factor 2, along with fasting insulin and glucose concentra tions, diastolic blood pressure, and waist girth. The observation that M loaded on both factors suggests that a resistance to insulin action may provide the mechanism uniting the features of the insulin resista nce syndrome. Hyperinsulinemia with concomitant insulin resistance may be necessary to produce this metabolic derangement, as well as the in creased risk of macrovascular complications.