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Proteomics Analysis of Platelets from Morbidly Obese Subjects
Author(s) -
Dobrydneva Yuliya,
Dutta Sucharita
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.805.4
Subject(s) - platelet , medicine , diabetes mellitus , platelet activation , endocrinology , insulin receptor , insulin , insulin resistance
Morbid obesity is accompanied by platelet hyperactivity and increased incidence of thrombosis. Proteomics studies were performed to characterize the effects of morbid obesity (BMI>35) on platelet protein profile. Platelets were isolated from morbidly obese subjects who do not have diabetes and who do not take medications affecting platelet function, and from lean individuals (controls) that are matched by sex, race and age to obese subjects. Platelet lysate was loaded into the LC‐MS/MS system following trypsin digestion. High resolution accurate Q‐Exactive instrument was used to identify and quantitate proteins. Pathway analysis was performed by Ingenuity. Comparing the proteomic profile between lean and obese individuals, we identified changed level of expression of several proteins that are implicated in diabetes signaling. These proteins include, among others, arachidonate 12‐lipoxygenase; insulin receptor, insulin receptor substrate 1, Akt; and CD36 (thrombospondin receptor). The molecular function category for the proteins that showed regulatory differences between the lean and obese were involved in carbohydrate metabolism, immune response, response to wounding and hemostasis pathways, among others. In summary, platelets from morbidly obese individuals who do not have diabetes nevertheless display changes consistent with defective insulin signaling and pro‐diabetic phenotype. Since insulin exerts inhibitory effect on platelet activation, dysregulation of this pathway may lead to prothrombotic state in morbid obesity.