Endocrine Abstracts (2006) 11 P343

Obesity and expression of serotonin transporter (SERT) in human platelets

A Marsili1, F Santini1, C Pelosini1, L Betti2, L Fabbrini2, G Galli1, I Ricco1, S Baroni2, P Italiani2, P Fierabracci1, G Giannaccini2 & A Pinchera1


1Dip. Endocrinologia, University of Pisa, Pisa, Italy; 2Dip. Psichiatria, Neurobiologia, Farmacologia e Biotecnologie, University of Pisa, Pisa, Italy.


Serotonergic transmission is involved in eating behaviour and body weight control. Comparison of SERT properties in blood platelets and serotonergic synaptosomes suggests that the human platelet can serve as an appropriate model for the transport, metabolism and release of serotonin by serotonergic neurons.Aim of this study was to evaluate SERT expression in platelets obtained from overweight or obese subjects (OB) as compared with normal weight healthy volunteers (C), and to look for possible correlations between SERT expression and various clinical or biochemical parameters. 34 OB (BMI range: 25–55) were compared with a group of C (BMI range: 18.5–24.9). SERT expression was evaluated in platelet membranes by the specific binding of [3H]paroxetine, and both maximal binding capacity (Bmax, fmol/mg protein) and dissociation constant (Kd, nM) were estimated. Results: Kd values in the two groups did not show significant difference. The mean Bmax of [3H]paroxetine was significantly lower in OB than in C (Bmax: 1083.23±276.9 vs 1443.8±242.55 fmol/mg protein, respectively, P<0.005). An inverse correlation was observed between BMI and Bmax values, as assessed by simple linear regression (R=−0.563; P<0.0001). A significant negative correlation was also found between SERT Bmax and waist circumference (P=0.0046; R=−0.424), hip circumference (P=0.0009; R=−0.49), sistolic blood pressure (P=0.0237; R=−0.341), fasting serum glucose (P=0.001; R=−0.479), insulin (P<0.0001; R=−0.626), tryglycerides (P=0.0071; R=−0.4) C reactive protein (P=0.01; R=−0.39), VES (P=0.021; R=−0.359), haptoglobin (P=0.0135; R=−0.37), leptin (P=0.0002; R=−0.535) and PAI-1(P<0.0001; R=−0.559), while a positive correlation was found between SERT Bmax and HDL cholesterol (P=0.026; R=0.338). After multivariate analysis only insulin and PAI-1 were correlated with SERT Bmax independently of BMI.

In conclusion, our results suggest that adipose tissue may regulate SERT density on platelets (and possibly on serotonergic neurons). This effect could be mediated by circulating molecules related to adiposity.