Three relatively simple metabolic markers can help identify overweight individuals who are sufficiently insulin resistant to be at increased risk for various adverse outcomes. In the absence of a standardized insulin assay, we suggest that the most practical approach to identify overweight individuals who are insulin resistant is to use the cut-points for either triglyceride concentration or the triglyceride-high-density lipoprotein cholesterol concentration ratio.

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A significant relationship exists between insulin resistance and plasma concentrations of ADMA. Pharmacological intervention with rosiglitazone enhanced insulin sensitivity and reduced ADMA levels. Increases in plasma ADMA concentrations may contribute to the endothelial dysfunction observed in insulin-resistant patients.

Insulin resistance and obesity are both associated with lower plasma adiponectin concentrations. Since insulin resistance and obesity are related, the extent to which the association of adiponectin with insulin resistance is dependent on its relationship with obesity is unclear. To address this issue, fasting plasma adiponectin concentrations were measured in 60 nondiabetic subjects, stratified into four equal groups on the basis of both their degree of adiposity and insulin resistance. Insulin resistance was quantified by determining the steadystate plasma glucose (SSPG) concentration in response to an infusion of octreotide, glucose, and insulin, and degree of adiposity was assessed by BMI. Subjects were defined as obese (BMI >30.0 kg/m 2 ) or nonobese (<27.0 kg/m 2 ) and as either insulin sensitive (SSPG <100 mg/dl) or insulin resistant (>190 mg/dl). Insulin-resistant subjects had significantly (P < 0.001) lower (mean ؎ SD) adiponectin concentrations, whether they were obese (17.1 ؎ 5.9 g/ml) or nonobese (16.3 ؎ 7.5 g/ml) as compared with either obese, insulin-sensitive (34.3 ؎ 13.1 g/ml) or nonobese, insulin-sensitive (29.8 ؎ 15.3 g/ml) subjects. Finally, adiponectin levels in insulinsensitive subjects varied to a significantly greater degree than in insulin-resistant subjects. These results suggest that adiponectin concentrations are more closely related to differences in insulin-mediated glucose disposal than obesity. Diabetes 53: [585][586][587][588][589][590] 2004 A n association between adipokines and insulin resistance has been noted in both diabetic and nondiabetic states (1-3). Of particular interest have been the recent demonstrations that adiponectin may play a direct role in determining insulinmediated glucose uptake (3-7). However, since adiponectin is the major adipokine secreted by fat cells and is closely linked to obesity (8,9), it is unclear to what extent the association of adiponectin with insulin resistance is independent of its relationship with obesity. Understanding this association is of importance because it may clarify mechanisms of insulin resistance and influence our understanding and use of therapeutic modalities, such as weight loss or exercise to enhance insulin sensitivity.Studies have documented that adiponectin concentrations are significantly related to various measures of body fat (8 -11) and that significant weight loss leads to a rise in adiponectin levels (9,10). However, it is possible that the relationship between obesity and adiponectin is due in part to metabolic changes frequently associated with obesity. For example, insulin resistance and hyperinsulinemia are frequently associated with obesity, and both decline with weight loss (12-14). Importantly, both in vitro and in vivo studies (15,16) have demonstrated that insulin itself may lead to downregulation of adiponectin secretion from fat cells. Moreover, several studies (15-17) have reported that improving insulin resistance and reducing insulin levels with an insulin-sensitizing agent markedly increases adipo...

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