Key result
Obesity was associated with decreased platelet l-arginine influx, NOS activity, and cGMP levels, along with platelet hyperaggregability, compared to normal weight subjects.
Why the study?
Does obesity alter the l-arginine-nitric oxide pathway and platelet aggregability in adults without other cardiovascular risk factors?
Case-Control (n=35)
Does obesity alter the l-arginine-nitric oxide pathway and platelet aggregability in adults without other cardiovascular risk factors?
Obesity is associated with diminished nitric oxide bioavailability, increased inflammation, and impaired antioxidant defense, contributing to platelet hyperaggregability and potential future cardiovascular complications.
May elevate thrombotic risk in obesity; hypothesis-generating and requires prospective validation before clinical adoption.
Epidemiological evidence has shown that platelet activation markers are consistently elevated in obesity, contributing to its prothrombotic state. In order to improve the understanding of the regulation of platelet function in obesity, the aim of this study was to investigate the l-arginine-nitric oxide (NO) pathway in obese adults without other cardiovascular risk factor. Seventeen obese (body mass index [BMI] 35.9±1.0 kg/m(2) ) and eighteen age-matched normal weight subjects (BMI 22.0±0.6 kg/m(2) ) were included in this study. l-arginine influx was measured with incubation of l-[(3) H]-arginine. NO synthase (NOS) and arginase activities were determined by the citrulline assay and the conversion of l-[(14) C]-arginine to [(14) C]-urea, respectively. Cyclic guanosine monophosphate (cGMP) content was evaluated by enzyme-linked immunosorbent assay. In addition, the study analyzed: platelet aggregation; intraplatelet antioxidant enzymes, via superoxide dismutase (SOD) and catalase activities; and systemic levels of l-arginine, fibrinogen, and C-reactive protein (CRP). Obese patients presented a significant decrease of platelet l-arginine influx, NOS activity, and cGMP levels, along with platelet hyperaggregability. On the presence of NO donor, platelet aggregation was similar between the groups. The fibrinogen and CRP systemic levels were significantly higher and SOD activity was reduced in obesity. No significant differences were observed in plasma levels of l-arginine and intraplatelet arginase and catalase activities between groups. The diminished NO bioavailability associated with inflammatory status and impaired enzymatic antioxidant defence may contribute to future cardiovascular complications in obesity.
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Leite et al. (2016) conducted a case-control in Obesity (n=35). Obesity vs. Normal weight was evaluated on Platelet l-arginine influx, NOS activity, cGMP levels, and platelet aggregation. Obesity was associated with decreased platelet l-arginine influx, NOS activity, and cGMP levels, along with platelet hyperaggregability, compared to normal weight subjects.
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