Markers of Inflammation and Cellular Adhesion Molecules in Relation to Insulin Resistance in Nondiabetic Elderly: The Rotterdam Study

Abstract

Insulin resistance, which is highly prevalent in the elderly, issuggested to be accompanied by an increased acute phase response. Untilnow, it is unclear whether cellular adhesion molecules are involved inthe clustering of insulin resistance.In the present study, we examined the relationship of insulin resistance(measured by postload insulin) with levels of markers of inflammationand cellular adhesion molecules in a random sample of 574 nondiabeticelderly men and women participating in the Rotterdam Study. Associationswere assessed by regression analysis, with In-insulin as the dependentvariable {[}regression coefficient (95% confidence interval)].In our population, insulin was strongly and significantly (P < 0.001)associated with the markers of inflammation C-reactive protein {[}1.52(0.96-2.08)], -1-antichymotrypsin {[}1.25 (0.82-1.69)], and IL-6{[}2.60 (1.69-3.52)], adjusted for age and gender. Associationsweakened, to some extent, after additional adjustment for measures ofobesity, smoking, and cardiovascular disease. Insulin was associatedwith the soluble intercellular adhesion molecule 1 {[}2.22 (1.29-3.16; P< 0.001)], whereas no association with the soluble vascular celladhesion molecule 1 was found. The strength of the associations ofinsulin with C-reactive protein, -1-antichymotrypsin, IL-6, andsoluble intercellular adhesion molecule 1, as assessed by standardizedregression coefficients, was comparable with the strength of theassociations of insulin with high-density lipoprotein cholesterol, bodymass index, and waist-to-hip ratio.The results of this population-based study indicate that low-gradeinflammation and the cellular adhesion molecule soluble intercellularadhesion molecule 1 are an integral part of insulin resistance innondiabetic elderly. These factors may contribute to the well-knownrelationship between insulin resistance and cardiovascular disease riskand might potentially become therapeutic targets in insulin resistantsubjects.