scholarly journals Effect of Asthma Gymnastic on Blood Nitric Oxide, Mood, Energy Expenditure and Sex Quality

2021 ◽  
Vol 41 (2) ◽  
pp. 118-128
Author(s):  
Ita Juliastuti ◽  
Suradi Suradi ◽  
Debree Septiawan
2018 ◽  
Vol 18 ◽  
pp. 120-133 ◽  
Author(s):  
Zoltán Péterfi ◽  
Imre Farkas ◽  
Raphael G.P. Denis ◽  
Erzsébet Farkas ◽  
Motokazu Uchigashima ◽  
...  

Author(s):  
Yusup Subagio Sutanto ◽  
Ita Juliastuti ◽  
Debree Septiawan ◽  
Dewi Nurul Makhabah ◽  
Suradi Suradi

2003 ◽  
Vol 284 (6) ◽  
pp. H2375-H2383 ◽  
Author(s):  
Jorge Guillermo Peralta ◽  
Paola V. Finocchietto ◽  
Daniela Converso ◽  
Francisco Schöpfer ◽  
Marı́a Cecilia Carreras ◽  
...  

To preserve thermoneutrality, cold exposure is followed by changes in energy expenditure and basal metabolic rate (BMR). Because nitric oxide (NO) modulates mitochondrial O2 uptake and energy levels, we analyzed cold effects (30 days at 4°C) on rat liver and skeletal muscle mitochondrial NO synthases (mtNOS) and their putative impact on BMR. Cold exposure delimited two periods: A ( days 1–10), with high systemic O2 uptake and weight loss, and B ( days 10–30), with lower O2 uptake and fat deposition. mtNOS activity and expression decreased in period A and then increased in period B by 60–100% in liver and skeletal muscle ( P< 0.05). Conversely, mitochondrial O2 uptake remained initially high in the presence of l-arginine and later fell by 30–50% ( P < 0.05). On this basis, the estimated fractional contribution of liver plus muscle to total BMR varied from 40% in period A to 25% in period B. The transitional modulation of mtNOS in rat cold acclimation could participate in adaptive responses that favor calorigenesis or conservative energy-saving mechanisms.


Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).


2020 ◽  
Vol 134 (5) ◽  
pp. 473-512 ◽  
Author(s):  
Ryan P. Ceddia ◽  
Sheila Collins

Abstract With the ever-increasing burden of obesity and Type 2 diabetes, it is generally acknowledged that there remains a need for developing new therapeutics. One potential mechanism to combat obesity is to raise energy expenditure via increasing the amount of uncoupled respiration from the mitochondria-rich brown and beige adipocytes. With the recent appreciation of thermogenic adipocytes in humans, much effort is being made to elucidate the signaling pathways that regulate the browning of adipose tissue. In this review, we focus on the ligand–receptor signaling pathways that influence the cyclic nucleotides, cAMP and cGMP, in adipocytes. We chose to focus on G-protein–coupled receptor (GPCR), guanylyl cyclase and phosphodiesterase regulation of adipocytes because they are the targets of a large proportion of all currently available therapeutics. Furthermore, there is a large overlap in their signaling pathways, as signaling events that raise cAMP or cGMP generally increase adipocyte lipolysis and cause changes that are commonly referred to as browning: increasing mitochondrial biogenesis, uncoupling protein 1 (UCP1) expression and respiration.


2001 ◽  
Vol 28 (5-6) ◽  
pp. 459-462
Author(s):  
Pini Orbach ◽  
Charles E Wood ◽  
Maureen Keller-Wood
Keyword(s):  

2001 ◽  
Vol 120 (5) ◽  
pp. A684-A684
Author(s):  
I DANIELS ◽  
I MURRAY ◽  
W GODDARD ◽  
R LONG

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