Leptin-dependent platelet aggregation in healthy, overweight and obese subjects

A. Corsonello, F. Perticone, A. Malara, D. De Domenico, S. Loddo, M. Buemi, R. Ientile, F. Corica

Research output: Contribution to journalArticlepeer-review


OBJECTIVE: To investigate the effects of leptin on platelet aggregation and platelet free calcium (Ca2+) concentrations, and the role of the long form of leptin receptor (ObRb) and the phospholipase C (PLC) in mediating leptin effects on platelet function. DESIGN: Cross-sectional, clinical study. SETTING: Outpatient's Service for Prevention and Treatment of Obesity at the University Hospital of Messina, Italy. SUBJECTS: A total of 19 healthy, 14 overweight, and 16 obese male subjects. MEASUREMENTS: ADP-induced platelet aggregation and platelet Ca2+ were measured after incubation of platelet-rich plasma with leptin alone 5-200 ng/ml, leptin 200ng/ml and anti-human leptin receptor long-form antibody (ObRb-Ab) 5-10 μl, or leptin 200 ng/ml and PLC inhibitor U73122 0.5-1 nmol/l. RESULTS: Platelet stimulation with leptin lead to a significant and dose-dependent increase in platelet aggregation in healthy subjects. This effect was blunted in overweight, and strongly reduced in obese subjects. Similarly, the incubation with leptin induced a significant and dose-dependent increase in platelet free calcium, which was blunted in overweight and obese patients. The effect of leptin on platelet aggregation and platelet Ca2+ was completely abated by the anti-ObRb-Ab and the PLC inhibitor U73122. CONCLUSIONS: Leptin produces a dose-dependent enhancement of ADP-induced platelet aggregation in humans. Platelet aggregation response to leptin is blunted, but not completely abolished in overweight/obese subjects, thus suggesting that platelet may represent a site of leptin resistance in human obesity. Leptin increases platelet free calcium in a dose-dependent manner. The inhibition of PLC completely abates the effect of leptin on both platelet aggregation and Ca2+ levels. These findings suggest that signaling pathway other than JAK-STAT tyrosine phosphorylation (ie PLC and calcium) may be involved in mediating the prothrombotic action of leptin.

Original languageEnglish
Pages (from-to)566-573
Number of pages8
JournalInternational Journal of Obesity
Issue number5
Publication statusPublished - May 1 2003


  • Leptin
  • Platelet aggregation

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Public Health, Environmental and Occupational Health
  • Endocrinology
  • Food Science
  • Endocrinology, Diabetes and Metabolism


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