scholarly journals Pulse Wave Analysis and Cardiac Autonomic Neuropathy in Type 1 Diabetes: A Report from the Pittsburgh Epidemiology of Diabetes Complications Study

2011 ◽  
Vol 13 (12) ◽  
pp. 1264-1268 ◽  
Author(s):  
Aaron M. Secrest ◽  
Sara L. Marshall ◽  
Rachel G. Miller ◽  
Catherine T. Prince ◽  
Trevor J. Orchard
2010 ◽  
Vol 213 (2) ◽  
pp. 469-474 ◽  
Author(s):  
Catherine T. Prince ◽  
Aaron M. Secrest ◽  
Rachel H. Mackey ◽  
Vincent C. Arena ◽  
Lawrence A. Kingsley ◽  
...  

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 548-P
Author(s):  
VALLIMAYIL VELAYUTHAM ◽  
PAUL Z. BENITEZ-AGUIRRE ◽  
MARIA E. CRAIG ◽  
JANINE CUSUMANO ◽  
GERALD LIEW ◽  
...  

2019 ◽  
Vol 16 (3) ◽  
pp. 297-299 ◽  
Author(s):  
Sharon Nina Admoni ◽  
Daniele Pereira Santos-Bezerra ◽  
Ricardo Vesoni Perez ◽  
Thiago Andrade Patente ◽  
Maria Beatriz Monteiro ◽  
...  

Cardiac autonomic neuropathy is a neglected diabetic chronic complication for which genetic predictors are rarely reported. Oxidative stress is implicated in the pathogenesis of microvascular complications, and glutathione peroxidase 4 is involved in the detoxification of peroxides and of reactive oxygen species. Thus, the association of a functional variant in the gene encoding glutathione peroxidase 4 (rs713041) with this diabetic complication was investigated in 341 individuals with type 1 diabetes evaluated for cardiac autonomic neuropathy status (61.7% women, 34 [27–42] years old; diabetes duration: 21 [15–27] years; HbA1c: 8.3% [7.4–9.4]; as median [interquartile interval]). Cardiac autonomic neuropathy was present in 29% of the participants. There was an inverse association of the minor T allele of rs713041 with cardiac autonomic neuropathy (odds ratio = 0.39; 95% confidence interval = 0.17–0.90; p  = 0.0271) after adjustment for potential confounders. The functional glutathione peroxidase 4 variant rs713041 modulated the risk for cardiac autonomic neuropathy in the studied population with type 1 diabetes.


2019 ◽  
Vol 57 (3) ◽  
pp. 271-278
Author(s):  
Jinghui Ju ◽  
Erin L. Tomaszewski ◽  
Trevor J. Orchard ◽  
Rhobert W. Evans ◽  
Eleanor Feingold ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Daniele P. Santos-Bezerra ◽  
Luciano R. Filgueiras ◽  
Maria Beatriz Monteiro ◽  
Sharon N. Admoni ◽  
Ricardo V. Perez ◽  
...  

Background and Aims. Since hyperglycemia promotes inflammation by different pathways and inflammation participates in the development of chronic diabetes complications, we investigated the association between the leukotriene (LT) pathway and microvascular diabetes complications. Methods and Results. Quantitative polymerase chain reaction was employed to quantify the expression of ALOX5 (encodes 5-lipoxygenase), LTB4R (encodes one of the LTB4 receptors), and MYD88 in peripheral blood mononuclear cells from 164 type 1 diabetes (T1D) individuals presenting or not diabetes kidney disease, retinopathy, peripheral neuropathy, and cardiovascular autonomic neuropathy (CAN); 26 nondiabetic subjects were included as controls. LTB4 plasmatic concentrations were also evaluated. The expression of LTB4R was significantly higher in T1D individuals than in controls. T1D individuals with microvascular complications presented lower MYD88 mRNA expression when compared to those without microvascular complications. Higher LTB4 concentrations were found in individuals with CAN versus without CAN. The observation of two distinct subgroups of T1D individuals in the correlation analyses motivated us to evaluate the characteristics of each one of these groups separately. The group presenting higher expression of ALOX5 and of LTB4R also presented higher values of HbA1C, of fructosamine, and of plasmatic LTB4. Conclusion. In the diabetes setting, the LT pathway is not only activated by hyperglycemia but is also modulated by the status of the autonomic nervous system.


2019 ◽  
Vol 10 (4) ◽  
pp. 985-989 ◽  
Author(s):  
Daniele Pereira Santos‐Bezerra ◽  
Sharon Nina Admoni ◽  
Rosana Cristina Mori ◽  
Tatiana Souza Pelaes ◽  
Ricardo Vesoni Perez ◽  
...  

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