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Nicotinamide-rich diet improves physical endurance by up-regulating SUR2A in the heart.

Sukhodub A, Sudhir R, Du Q, Jovanović S, Reyes S, Jovanović A - J. Cell. Mol. Med. (2011)

Bottom Line: We have found that mice on nicotinamide-rich diet significantly improved physical endurance, which was associated with significant increase in expression of SUR2A.The experiments focused on action membrane potential and intracellular Ca(2+) concentration have demonstrated that increased SUR2A expression was associated with the activation of sarcolemmal K(ATP) channels and steady Ca(2+) levels in cardiomyocytes in response to β-adrenergic stimulation.The obtained results suggest that oral nicotinamide is a regulator of SUR2A expression and has a potential as a drug that can improve physical endurance in conditions where this effect would be desirable.

View Article: PubMed Central - PubMed

Affiliation: Division of Medical Sciences, Centre for Cardiovascular and Lung Biology, Ninewells Hospital & Medical School, University of Dundee, Dundee, UK.

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Physical endurance in mice on control and nicotinamide-rich diet. Bar graphs showing energy expenditure (A) and time spent (B) on treadmill of mice on control and nicotinamide-rich diet. Each bar represents mean ± S.E. of the mean (n = 6). *P < 0.05.
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fig03: Physical endurance in mice on control and nicotinamide-rich diet. Bar graphs showing energy expenditure (A) and time spent (B) on treadmill of mice on control and nicotinamide-rich diet. Each bar represents mean ± S.E. of the mean (n = 6). *P < 0.05.

Mentions: To test physical endurance of mice on control and nicotinamide-rich diet, we have used treadmill as described previously [13]. The tolerated workload, a parameter that incorporates time of effort with speed and incline of the treadmill, was significantly higher in mice on nicotinamide-rich diet compared with the mice on control diet (tolerated workload was 54.7 ± 5.1 J in mice on control and 104 ± 8.2 J in mice on nicotinamide-rich diet, n = 6 for each, P < 0.01; Fig. 3). Mice on control diet were able to stay on treadmill for 67.3 ± 6.2 min. (n = 6), while this time was significantly increased in mice on nicotinamide-rich diet (to 144.0 ± 14.9 min.; Fig. 3; P < 0.01).


Nicotinamide-rich diet improves physical endurance by up-regulating SUR2A in the heart.

Sukhodub A, Sudhir R, Du Q, Jovanović S, Reyes S, Jovanović A - J. Cell. Mol. Med. (2011)

Physical endurance in mice on control and nicotinamide-rich diet. Bar graphs showing energy expenditure (A) and time spent (B) on treadmill of mice on control and nicotinamide-rich diet. Each bar represents mean ± S.E. of the mean (n = 6). *P < 0.05.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4373361&req=5

fig03: Physical endurance in mice on control and nicotinamide-rich diet. Bar graphs showing energy expenditure (A) and time spent (B) on treadmill of mice on control and nicotinamide-rich diet. Each bar represents mean ± S.E. of the mean (n = 6). *P < 0.05.
Mentions: To test physical endurance of mice on control and nicotinamide-rich diet, we have used treadmill as described previously [13]. The tolerated workload, a parameter that incorporates time of effort with speed and incline of the treadmill, was significantly higher in mice on nicotinamide-rich diet compared with the mice on control diet (tolerated workload was 54.7 ± 5.1 J in mice on control and 104 ± 8.2 J in mice on nicotinamide-rich diet, n = 6 for each, P < 0.01; Fig. 3). Mice on control diet were able to stay on treadmill for 67.3 ± 6.2 min. (n = 6), while this time was significantly increased in mice on nicotinamide-rich diet (to 144.0 ± 14.9 min.; Fig. 3; P < 0.01).

Bottom Line: We have found that mice on nicotinamide-rich diet significantly improved physical endurance, which was associated with significant increase in expression of SUR2A.The experiments focused on action membrane potential and intracellular Ca(2+) concentration have demonstrated that increased SUR2A expression was associated with the activation of sarcolemmal K(ATP) channels and steady Ca(2+) levels in cardiomyocytes in response to β-adrenergic stimulation.The obtained results suggest that oral nicotinamide is a regulator of SUR2A expression and has a potential as a drug that can improve physical endurance in conditions where this effect would be desirable.

View Article: PubMed Central - PubMed

Affiliation: Division of Medical Sciences, Centre for Cardiovascular and Lung Biology, Ninewells Hospital & Medical School, University of Dundee, Dundee, UK.

Show MeSH