Affiliations: Département de Physiologie, Institut de Biologie, Faculté de Medecine, 34060 Montpellier, France
Abstract: Metabolic modifications associated with the syndrome ‘X’ of Reaven (insulin resistance-hyperinsulinemia syndrome) might explain at least in part the rheologic changes of obesity. This hypothesis was investigated in 101 subjects (38 overweight (Ob+), 22 obese (Ob++) and 41 controls) during a standardized breakfast test. Baseline values of plasma viscosity (μpl), blood viscosity at high shear rate, RBC filterability (Hanss' hemorheometre), hematocrit, RBC aggregation (Myrenne aggregometer) serum cholesterol and triglycerides were measured. When compared to controls, obese patients Ob+ and Ob++ had a higher hematocrit (+2.5 % p<0.02). Plasma viscosity was similar in the three groups. Blood viscosity (at both native and corrected (45%) hematocrit) is higher in Ob++ (repectively p<0.01 and p<0.04) while Ob+ have values similar to controls. The ratio of blood viscosity (at corrected hematocrit 45%) on plasma viscosity which is related to RBC deformability is higher in Ob++ (p<0.02). On the whole group of subjects (n=101) blood viscosity (at corrected hematocrit 45%) was correlated to baseline insulinemia (r=0.225 p<0.03) and triglyceridemia (r=0.228 p<0.02), but it failed to be correlated to blood pressure in obese subjects. Serum cholesterol was correlated to RBC rigidity in controls. RBC aggregation ‘M’ index was correlated with body mass index (r=0.265 n=88 p=0.0124), cholesterol (r=0.21 n=88 p=0.0462), baseline insulinemia (r=0.37 n=83 p=0.0007) and fibrinogen (r=0.35 n=40 p=0.028). ‘M1’ index was correlated to triglycerides (r=0.21 n=88 p=0.045) and baseline insulinemia (r=0.24 n=83 p=0.0322). These findings suggest that (a) the main hemorheologic disorders in obese are a higher hematocrit and RBC rigidity; (b) metabolic disorders (hyperinsulinemia, hypertriglyceridemia, i.e. signs of the ‘X’ syndrome of Reaven) are associated with hyperviscosity; (c) thus, we hypothesize that hyperviscosity may be a mechanism involved in the vascular risk of hyperinsulinemia (or a marker of such a risk).
