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Isolation, Expansion, and Adipogenic Induction of CD34+CD31+ Endothelial Cells from Human Omental and Subcutaneous Adipose Tissue
Published on: July 17, 2018
Correlation between blood cell indices and adiponectin and leptin levels in COVID-19
Mia Manojlovic1, Branislava Ilincic2, Marko Bojovic3
1University of Novi Sad, Faculty of Medicine in Novi Sad, Novi Sad, Serbia; Clinic for Endocrinology, Diabetes and Metabolic Disorders, University Clinical Center of Vojvodina, Novi Sad, Serbia.
Abstract:
Adipose tissue (AT) is a major metabolic organ, functioning through autocrine, paracrine, and endocrine mechanisms. This study investigated the relationship between adipokine levels and blood cell indices, particularly platelets, in individuals with COVID-19. Another aim was to enhance the understanding of AT's endocrine function during dynamic pathological changes, such as acute viral infections like COVID-19. The study was conducted as a cross-sectional analysis at the University Clinical Center of Vojvodina in 2021 and 2022, including 76 consecutive SARS-CoV-2-positive patients of both sexes. Study parameters were determined from peripheral venous blood samples routinely collected upon hospital admission. The results showed that leptin levels were significantly positively correlated with body mass index (BMI) (ρ = 0.421, P < 0.001) and body fat mass (BFM) (ρ = 0.547, P < 0.001). Simultaneously, a significant negative correlation was observed between adiponectin levels and BMI (ρ = -0.430, P < 0.001). Additionally, a significant positive correlation was found between leptin levels and mean platelet volume (MPV) (ρ = 0.307, P < 0.05), platelet distribution width (PDW) (ρ = 0.325, P < 0.05), and platelet-large cell ratio (P-LCR) (ρ = 0.305, P < 0.05). Leptin's impact on platelet indices was confirmed in both simple and multiple linear regression models, where leptin exhibited a slightly higher beta coefficient than BMI. In contrast, adiponectin levels were negatively correlated with hematocrit (HCT) (ρ = -0.329, P < 0.05). These findings may provide further insight into the previously suspected role of AT in the complex cascade of COVID-19 pathogenesis and platelet activation.
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