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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 wild-type (WT) and SUR2A mice on control diet. Bar graphs showing energy expenditure (A) and time spent (B) on treadmill of WT and SUR2A mice. Each bar represents mean ± S.E. of the mean (n = 6). *P < 0.05.
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fig04: Physical endurance in wild-type (WT) and SUR2A mice on control diet. Bar graphs showing energy expenditure (A) and time spent (B) on treadmill of WT and SUR2A mice. Each bar represents mean ± S.E. of the mean (n = 6). *P < 0.05.

Mentions: To determine whether a sole increase in SUR2A would have similar effect on physical endurance as a nicotinamide-rich diet, we have taken advantage of transgenic phenotype overexpressing SUR2A alone [19]. Under the exercise-stress test, mice in which the SUR2A was under control of cytomegalovirus promoter performed at a significantly increased level than the littemate controls (Fig. 4). The tolerated workload was ∼2-fold higher in transgenic mice compared with the wild-type animals (tolerated workload was 45.6 ± 2.2 J in wild-type mice and 91.6 ± 13.4 J in SUR2A mice, n = 5–7, P = 0.01; Fig. 4). Time spent on treadmill was significantly increased in SUR2A mice when compared to the wild-type (Fig. 4).


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 wild-type (WT) and SUR2A mice on control diet. Bar graphs showing energy expenditure (A) and time spent (B) on treadmill of WT and SUR2A mice. 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

fig04: Physical endurance in wild-type (WT) and SUR2A mice on control diet. Bar graphs showing energy expenditure (A) and time spent (B) on treadmill of WT and SUR2A mice. Each bar represents mean ± S.E. of the mean (n = 6). *P < 0.05.
Mentions: To determine whether a sole increase in SUR2A would have similar effect on physical endurance as a nicotinamide-rich diet, we have taken advantage of transgenic phenotype overexpressing SUR2A alone [19]. Under the exercise-stress test, mice in which the SUR2A was under control of cytomegalovirus promoter performed at a significantly increased level than the littemate controls (Fig. 4). The tolerated workload was ∼2-fold higher in transgenic mice compared with the wild-type animals (tolerated workload was 45.6 ± 2.2 J in wild-type mice and 91.6 ± 13.4 J in SUR2A mice, n = 5–7, P = 0.01; Fig. 4). Time spent on treadmill was significantly increased in SUR2A mice when compared to the wild-type (Fig. 4).

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