Relationships between metabolic and hemorheologic modifications associated with overweight

Abstract

Faculte de Medecine, 34060 Montpelliel', France (Received 14.9.1991; accepted 14.11.1992) Metabolic modifications associated with the syndrome 'X' of Reaven (insulin resistance-hyperinsulinemja syndrome) might explain at least in par:t the rheologic changes of obesity. This hypothesis was investigated in 101 subjects (38 overweight (Ob+), 22 obese (Ob++) and 41 controls) during a standardiz.ed breakfast test. Baseline values of plasma viscosity (lIpl), blood viscosity at high shear rate, RBe filterability (Hanss' hemorheometre), hematocrit, RBe aggregation (Myrenne aggregometer) serum cholesterol and triglycerides were measured. When compared to controls, obese patients Ob+ and Ob++ had a higher he,atocrit (+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<O.04) while Ob+ have values similar to controls. The ratio of blood viscosity (at corrected hematocrit 45%) on plasma viscosity which is related to RBe 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 irpsulinemia (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 RBe rigidity in controls. RBe 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=O.0322). These findings suggest that (a) the main hemorheologic disorders in obese are a higher hematocrit and RBe rigidity; (b) metabolic disorders (hyperjnsulinemia, 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).