scholarly journals Cardiovascular Disease Risk Factors and Platelet Mitochondrial Function in School Age Children (P21-059-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Eva Diaz Fuentes ◽  
Sean Adams ◽  
Catarina Young ◽  
Judith Weber ◽  
Elisabet Borsheim

Abstract Objectives Platelets (PL) are an accessible source of human mitochondria. Thus, PL are advantageous when studying mitochondrial function in vulnerable populations. The objective of this study was to measure the association between parameters of PL mitochondrial respiration and markers of cardiovascular disease risk [adiposity, fitness and blood pressure (BP)] in a sub-sample of school age children participants of a larger study called Arkansas Active Kids. Methods After overnight fasting, body composition (DXA), VO2peak (incremental cycle ergometer test), resting BP, and mitochondrial function of permeabilized platelets (high-resolution respirometry) were measured in 46 children. Routine respiration (R), fatty acid oxidation (F = octanoylcarnitine + ADP + malate), respiratory stimulation by simultaneous action of F plus NADH-linked complex (C) I substrates (F&CI = pyruvate, malate and glutamate), succinate (F&CI&CII), and glycerolphosphate (F&CI&CII&GpDH) were measured. Noncoupled electron transfer capacity (ETE, FCCP), CIIE&GpDHE respiration (rotenone), residual oxygen consumption (ROX, antimycin) and CIV activity were also measured. Flux control ratios were computed by normalizing to ET capacity in the presence of NADH-linked substrates. Data presented as mean ± SD and Spearman correlations (Rho). Results Children were 9 ± 1 years with an average BMI percentile (BMIp) of 59 ± 30, and % fat mass (%FM) of 33 ± 6% (range: 25 to 49%). Ten children (22%) had either elevated or stage 1 hypertension as defined by the American Academy of Pediatrics. Diastolic BP percentile, VO2peak (ml·kg−1 fat-free-mass−1), BMIP, and % fat mass (%FM) did not correlate with any parameter of platelet mitochondrial respiration. However, visceral fat area (cm2) correlated with FAO (Rho = 0.35, P = 0.017) and F&CI (Rho = 0.30, P = 0.043) while systolic BP correlated with F&CI&CII&GpDH (Rho = 0.31, P = 0.037) and ETE (Rho = 0.43, P = 0.003). Conclusions In this preliminary analysis, PL fatty acid oxidation of school-age children increased with increasing visceral adiposity while the convergent electron flow through the Q-junction increased with increasing systolic blood pressure. Funding Sources USDA 59-6250-4-001; NIH P20GM109096. USDA/ARS Project 6026-51000-010-05S.

2010 ◽  
Vol 110 (2) ◽  
pp. 253-260 ◽  
Author(s):  
Otilia Perichart-Perera ◽  
Margie Balas-Nakash ◽  
Ameyalli Rodríguez-Cano ◽  
Cinthya Muñoz-Manrique ◽  
Adriana Monge-Urrea ◽  
...  

2018 ◽  
Vol 10 (7) ◽  
pp. 4643-4652 ◽  
Author(s):  
Drew B. Day ◽  
Merlise A. Clyde ◽  
Jianbang Xiang ◽  
Feng Li ◽  
Xiaoxing Cui ◽  
...  

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
J. Ruth Wu-Wong ◽  
William Noonan ◽  
Masaki Nakane ◽  
Kristin A. Brooks ◽  
Jason A. Segreti ◽  
...  

Endothelial dysfunction increases cardiovascular disease risk in chronic kidney disease (CKD). This study investigates whether VDR activation affects endothelial function in CKD. The 5/6 nephrectomized (NX) rats with experimental chronic renal insufficiency were treated with or without paricalcitol, a VDR activator. Thoracic aortic rings were precontracted with phenylephrine and then treated with acetylcholine or sodium nitroprusside. Uremia significantly affected aortic relaxation (% in NX rats versus % in SHAM at 30 M acetylcholine). The endothelial-dependent relaxation was improved to –%, –%, and –% in NX rats treated with paricalcitol at 0.021, 0.042, and 0.083 g/kg for two weeks, respectively, while paricalcitol at 0.042 g/kg did not affect blood pressure and heart rate. Parathyroid hormone (PTH) suppression alone did not improve endothelial function since cinacalcet suppressed PTH without affecting endothelial-dependent vasorelaxation. N-omega-nitro-L-arginine methyl ester completely abolished the effect of paricalcitol on improving endothelial function. These results demonstrate that VDR activation improves endothelial function in CKD.


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