There are some reports concerning the relationship between insulin sensitivity and whole-blood viscosity calculated 1,2 or measured. 3,4 On the other hand we know that in obese subjects, characterized by an alteration of insulin sensitivity, a hyperviscosity condition is present and that in these subjects weight reduction especially affects plasma viscosity and not the other haemorheological determinants. 5,6 We examined, in a group of subjects with metabolic syndrome (MS) defined according to the WHO criteria, 7 the relationship between plasma viscosity and the parameters reflecting insulin-resistance.In 19 subjects with MS (nine men and 10 women; mean age 49.0 AE 10.2 y body mass index (BMI) 33.3 AE 4.5 kg=m 2 waist -hip ratio (WHR) 0.915 AE 0.071; systolic blood pressure 135.8 AE 19.3 mmHg; diastolic blood pressure 83.4 AE 6.2 mmHg; fasting blood glucose level 9.12 AE 3.56 mmol=l; Hb Alc 7.06 AE 1.84%; microalbuminuria 5.7 AE 3.2 ng=min), the insulin sensitivity was assessed by performing a euglycaemic hyperinsulinaemic clamp and considering the glucose disposal (M), expressed as mg=kg=min and calculated on the basis of the glucose amount infused, and the glucose metabolic clearance rate (MCR), expressed as ml=kg=min and calculated by dividing the amount of metabolized glucose (M) by the plasma glucose concentration. In these subjects, plasma viscosity (PV) was determined on fasting venous blood anticoagulated with ethylenediaminetetracetate (EDTA), at the shear rate of 450 s 71 , using the viscosimeter Wells-Brookfield 1 2 LVT. Between normal subjects and patients with MS there was a significant difference in plasma viscosity (n ¼ 1.24 AE 0.08, MS ¼ 1.40 AE 0.10, P < 0.001). This haemorheological parameter was negatively correlated to the values of M (r 2 ¼ 0.398, P < 0.01) and MCR (r 2 ¼ 0.370, P < 0.01).We then observed that the trend of the PV is related to both parameters reflecting the insulin-resistance, revealing how its behaviour is influenced by the degree of resistance. Besides considering the PV another component of the MS, our interest in underlining these relationships was motivated by the consideration that insulin-resistance and PV impair the microhaemodynamic pattern, and this impairment may be one of the links not only between insulin-resistance and the principal features (diabetes mellitus, hypertension, obesity etc) of MS, but also between insulin-resistance and the vascular complications accompanying this syndrome.