title: Reactive leptin resistance and the profile of platelet activation in acute ischaemic stroke patients.
abstract: Leptin is an adipokine that in vitro enhances agonist-induced platelet aggregation and adipokine expression. Hyperleptinaemia represents a risk factor for cardiovascular disease. We conducted a prospective evaluation of the potential link between blood platelet activation and plasma leptin levels in post-stroke patients. Using five-colour flow cytometry, the platelet surface expression of CD40L, CD62P, the subpopulations of monocyte-platelet aggregates and platelet-derived microparticles (PMPs) as well as the plasma leptin, soluble leptin receptor (sOb-R), leptin/sOb-R ratio, the plasma adiponectin, and leptin/adiponectin ratio were assessed in 98 stroke patients on the first (V₀), 10th (V₁ ) and 90th (V₂) day after stroke and once in 78 age-, gender- and vascular risk factor-matched disease controls. We demonstrated that at V0 leptin resistance, defined as leptin/sOb-R ratio, was higher than in the controls [1.1 (0.5-1.8 vs. 0.5 (0.2-1.1); p=0.02]. After adjustment according to the factors which influence platelet activation, we confirmed the relationship between percentage of circulating PMPs and plasma leptin level (B=0.18; p=0.02) or the leptin/sOb-R ratio (B=0.23; p=0.02) in normal-weight subjects in the acute phase of stroke. No correlation could be demonstrated between the adipokine parameters and the percentage of monocyte-platelet aggregates or expression of platelet pro-inflammatory glycoproteins. In conclusion, formation of PMPs on the first day following an ischaemic stroke shows a positive correlation with leptin levels and with resistance to leptin. Leptin level does not seem to affect the expression of platelet surface proinflammatory glycoproteins.
authors.affiliation: Department of Neurology, Poznan University of Medical Sciences, ul. Przybyszewskiego 49, 60-355 Poznan, Poland. mlukasik@ump.edu.pl
authors.forename: Maria
authors.initials: M
authors.lastname: Lukasik
authors.forename: Slawomir
authors.initials: S
authors.lastname: Michalak
authors.forename: Grzegorz
authors.initials: G
authors.lastname: Dworacki
authors.forename: Karolina
authors.initials: K
authors.lastname: Siewiera
authors.forename: Mariusz
authors.initials: M
authors.lastname: Kaczmarek
authors.forename: Cezary
authors.initials: C
authors.lastname: Watala
authors.forename: Wojciech
authors.initials: W
authors.lastname: Kozubski
mesh_terms: D000208:Acute Disease; D052242:Adiponectin / Q000097:blood; D000368:Aged; D001792:Blood Platelets / Q000378:metabolism* / Q000473:pathology; D023201:CD40 Ligand / Q000378:metabolism; D002469:Cell Separation; D055252:Cell-Derived Microparticles / Q000473:pathology; D018450:Disease Progression; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D020738:Leptin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism / Q000473:pathology; D019007:P-Selectin / Q000378:metabolism; D015539:Platelet Activation; D011446:Prospective Studies; D020521:Stroke / Q000175:diagnosis* / Q000473:pathology / Q000503:physiopathology
chemical_list: D052242:Adiponectin; D020738:Leptin; D019007:P-Selectin; D023201:CD40 Ligand