scholarly journals Effect of diet and age on expression of renal NOS isoforms and splicing in female Zucker rats

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Yuriy Slyvka ◽  
Sharon R Inman ◽  
Felicia V Nowak
Keyword(s):  
Zucker Rats ◽  
Nos Isoforms

scholarly journals Renal NOS isoforms and splicing in 13 week obese female Zucker rats on antioxidant vs regular diet

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Sharon R Inman ◽  
Yuriy Slyvka ◽  
Yelena Feldman ◽  
Felicia V Nowak
Keyword(s):  
Zucker Rats ◽  
Regular Diet ◽  
Obese Female ◽  
Nos Isoforms

Insulin regulated aminopeptidase (IRAP) inhibition affects glucose metabolism in obese pre-diabetic Zucker rats

2020 ◽  
Author(s):  
Katarina Krskova ◽  
Lucia Balazova ◽  
Viktoria Dobrocsyova ◽  
Erika Balogova ◽  
Maciej Suski ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Zucker Rats

Altered neuropeptide Y concentrations in specific hypothalamic regions of obese (fa/fa) Zucker rats. Possible relationship to obesity and neuroendocrine disturbances

Diabetes ◽  
1991 ◽  
Vol 40 (11) ◽  
pp. 1423-1429 ◽  
Author(s):  
P. E. McKibbin ◽  
S. J. Cotton ◽  
S. McMillan ◽  
B. Holloway ◽  
R. Mayers ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Zucker Rats

Targeting the Endothelial Ca2+ Toolkit to Rescue Endothelial Dysfunction in Obesity Associated-Hypertension

2020 ◽  
Vol 27 (2) ◽  
pp. 240-257 ◽  
Author(s):  
Francesco Moccia ◽  
Sharon Negri ◽  
Pawan Faris ◽  
Roberto Berra-Romani
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Endothelial Damage ◽  
Vascular Damage ◽  
Zucker Rats ◽  
Bibliographic Databases ◽  
Resistance Arteries ◽  
Small Resistance ◽  
Obese Zucker Rats ◽  
Transient Receptor

Background: Obesity is a major cardiovascular risk factor which dramatically impairs endothelium- dependent vasodilation and leads to hypertension and vascular damage. The impairment of the vasomotor response to extracellular autacoids, e.g., acetylcholine, mainly depends on the reduced Nitric Oxide (NO) bioavailability, which hampers vasorelaxation in large conduit arteries. In addition, obesity may affect Endothelium-Dependent Hyperpolarization (EDH), which drives vasorelaxation in small resistance arteries and arterioles. Of note, endothelial Ca2+ signals drive NO release and trigger EDH. Methods: A structured search of bibliographic databases was carried out to retrieve the most influential, recent articles on the impairment of vasorelaxation in animal models of obesity, including obese Zucker rats, and on the remodeling of the endothelial Ca2+ toolkit under conditions that mimic obesity. Furthermore, we searched for articles discussing how dietary manipulation could be exploited to rescue Ca2+-dependent vasodilation. Results: We found evidence that the endothelial Ca2+ could be severely affected by obese vessels. This rearrangement could contribute to endothelial damage and is likely to be involved in the disruption of vasorelaxant mechanisms. However, several Ca2+-permeable channels, including Vanilloid Transient Receptor Potential (TRPV) 1, 3 and 4 could be stimulated by several food components to stimulate vasorelaxation in obese individuals. Conclusion: The endothelial Ca2+ toolkit could be targeted to reduce vascular damage and rescue endothelium- dependent vasodilation in obese vessels. This hypothesis remains, however, to be probed on truly obese endothelial cells.

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