32 A 75 g OGTT was performed with basal and 2-hour postload sampling for plasma glucose assays. A value of pulse pressure ≥60 mm Hg was used as index of increased vascular stiffness. Pulse pressure was calculated as the difference between systolic blood pressure and diastolic blood pressure. Blood pressure was measured after a 5 min rest at the right upper arm, in the sitting position, with a sphygmomanometer for three times and the mean was used in the analyses. The BMI was calculated as body weight in kilograms divided by height in square meters (kg/m 2).

Waist circumference was measured at the umbilical level, at the midpoint between the iliac crest and the rib cage. Height was measured to the nearest 0.1 cm, while body weight was measured with a calibrated electronic scale to the nearest 0.1 kg. 3 31 On the first day, after an overnight fasting, all subjects underwent anthropometrical evaluation including measurements of body mass index (BMI), waist circumference, and body composition evaluated by bioelectrical impedance. The study sample includes 631 adults (age >18 years) consecutively recruited at the Department of Systems Medicine, University of Tor Vergata, Rome, and at the Department of Medical and Surgical Sciences of the University ‘Magna Graecia’ of Catanzaro, Italy, according to a previously described protocol. In the present study, we pursued two aims: (1) to compare VAI, LAP, TyG, and TG/HDL-C ratio surrogate indexes with the euglycemic hyperinsulinemic clamp method, the gold standard measure of insulin sensitivity, in a large cohort of European individuals with different degrees of glucose tolerance, and (2) to examine the relationship of surrogate measures of insulin sensitivity with classical and inflammatory cardiovascular risk factors, as well as carotid intima-media thickness (IMT), a reliable index of subclinical atherosclerosis 29 related to insulin resistance. 28 Although these two lipid-based surrogate indexes have been studied in non-diabetic individuals, in subjects with impaired fasting glucose (IFG), and in patients with type 2 diabetes, 26–28 it is unknown whether they might be useful in the identification of insulin resistance in individuals with impaired glucose tolerance (IGT). 18–25 Additionally, two other surrogate indexes of insulin sensitivity based on plasma triglyceride (TG) and high-density lipoprotein cholesterol (HDL-C) measurements, that is, the triglycerides × fasting glucose (TyG) index and TG/HDL-C concentration ratio, have been suggested as surrogate estimates of insulin sensitivity, and validated in comparison to the euglycemic hyperinsulinemic clamp method, 26 the steady-state plasma glucose (SSPG) concentration during the insulin suppression test 27 or a 3-hour hyperglycemic clamp test. Among these, the visceral adiposity index (VAI), 16 and the lipid accumulation product (LAP), both based on anthropometric and laboratory parameters 17 have been developed and analyzed in relation to homeostatic model assessment of insulin resistance (HOMA-IR), but not to the gold standard measure of insulin sensitivity assessed by the euglycemic hyperinsulinemic clamp method. 13–15 An ideal surrogate index of insulin sensitivity for use in large epidemiological studies should be based on affordable anthropometric and/or laboratory measures routinely gathered in clinical settings. Therefore, many surrogate indexes of insulin sensitivity have been proposed using anthropometric variables, fasting insulin and/or glucose levels or insulin and glucose levels during an oral glucose tolerance test (OGTT). 9–11 Although insulin resistance is an important determinant of cardiometabolic diseases, a direct measure of insulin sensitivity by the gold standard euglycemic hyperinsulinemic clamp technique 12 is impractical for large-scale epidemiological studies, due to the laborious, expensive, and time-consuming procedure required. 4–6 Insulin resistance is considered central to the pathophysiology of type 2 diabetes, 7 8 and predicts the development of cardiovascular disease. Insulin resistance is a characteristic trait of both pre-diabetes 1–3 and metabolic syndrome.

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