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Increasing muscle mass improves vascular function in obese (db/db) mice.

Qiu S, Mintz JD, Salet CD, Han W, Giannis A, Chen F, Yu Y, Su Y, Fulton DJ, Stepp DW - J Am Heart Assoc (2014)

Bottom Line: Inactivity is associated with a loss of muscle mass, which is also reversed with isometric exercise training.This impairment was improved by superoxide dismutase mimic Tempol.This improvement was blunted by nitric oxide (NO) synthase inhibitor l-NG-nitroarginine methyl ester (l-NAME).

View Article: PubMed Central - PubMed

Affiliation: Vascular Biology Center and Department of Physiology, Georgia Regents University, Augusta, GA, Germany (S.Q., J.D.M., C.D.S., W.H., A.G., F.C., Y.Y., Y.S., D.J.F., D.W.S.).

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eNOS expression in db/db mice was not decreased, compared to lean mice. A, Representative blot of phosphorylation of eNOS at Ser1177 and eNOS expression in mesenteric arteries. B and C, Quantification of eNOS (normalized to GAPDH) and phosphorylation of eNOS (normalized to total NOS) protein expression. Results are presented as mean±SEM. A through C, n>6; *P<0.05, db/db versus db/db myostatin−/−; ##P<0.01, lean versus db/db. db/db myostatin−/− indicates mice lacking both myostatin and leptin receptor; db/db, obese leptin receptor‐deficient mice heterozygous for myostastin; eNOS, endothelial nitric oxide synthase; lean myostatin−/−, myostatin‐ mice heterozygous for leptin receptors; lean, lean dual heterozygotes.
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fig09: eNOS expression in db/db mice was not decreased, compared to lean mice. A, Representative blot of phosphorylation of eNOS at Ser1177 and eNOS expression in mesenteric arteries. B and C, Quantification of eNOS (normalized to GAPDH) and phosphorylation of eNOS (normalized to total NOS) protein expression. Results are presented as mean±SEM. A through C, n>6; *P<0.05, db/db versus db/db myostatin−/−; ##P<0.01, lean versus db/db. db/db myostatin−/− indicates mice lacking both myostatin and leptin receptor; db/db, obese leptin receptor‐deficient mice heterozygous for myostastin; eNOS, endothelial nitric oxide synthase; lean myostatin−/−, myostatin‐ mice heterozygous for leptin receptors; lean, lean dual heterozygotes.

Mentions: To determine the role of eNOS in the observed results, eNOS expression was determined by Western blotting. As shown in Figure 9, total eNOS protein expression was elevated in obesity and partially normalized with myostatin deletion. The increased eNOS was likely a compensation for another deficit that was normalized by myostatin deletion (ie, superoxide). Phosphorylation state of eNOS was assessed with Abs to serine 1177 of eNOS. There was no effect of either obesity or myostatin deletion on eNOS phosphorylation expression.


Increasing muscle mass improves vascular function in obese (db/db) mice.

Qiu S, Mintz JD, Salet CD, Han W, Giannis A, Chen F, Yu Y, Su Y, Fulton DJ, Stepp DW - J Am Heart Assoc (2014)

eNOS expression in db/db mice was not decreased, compared to lean mice. A, Representative blot of phosphorylation of eNOS at Ser1177 and eNOS expression in mesenteric arteries. B and C, Quantification of eNOS (normalized to GAPDH) and phosphorylation of eNOS (normalized to total NOS) protein expression. Results are presented as mean±SEM. A through C, n>6; *P<0.05, db/db versus db/db myostatin−/−; ##P<0.01, lean versus db/db. db/db myostatin−/− indicates mice lacking both myostatin and leptin receptor; db/db, obese leptin receptor‐deficient mice heterozygous for myostastin; eNOS, endothelial nitric oxide synthase; lean myostatin−/−, myostatin‐ mice heterozygous for leptin receptors; lean, lean dual heterozygotes.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4309080&req=5

fig09: eNOS expression in db/db mice was not decreased, compared to lean mice. A, Representative blot of phosphorylation of eNOS at Ser1177 and eNOS expression in mesenteric arteries. B and C, Quantification of eNOS (normalized to GAPDH) and phosphorylation of eNOS (normalized to total NOS) protein expression. Results are presented as mean±SEM. A through C, n>6; *P<0.05, db/db versus db/db myostatin−/−; ##P<0.01, lean versus db/db. db/db myostatin−/− indicates mice lacking both myostatin and leptin receptor; db/db, obese leptin receptor‐deficient mice heterozygous for myostastin; eNOS, endothelial nitric oxide synthase; lean myostatin−/−, myostatin‐ mice heterozygous for leptin receptors; lean, lean dual heterozygotes.
Mentions: To determine the role of eNOS in the observed results, eNOS expression was determined by Western blotting. As shown in Figure 9, total eNOS protein expression was elevated in obesity and partially normalized with myostatin deletion. The increased eNOS was likely a compensation for another deficit that was normalized by myostatin deletion (ie, superoxide). Phosphorylation state of eNOS was assessed with Abs to serine 1177 of eNOS. There was no effect of either obesity or myostatin deletion on eNOS phosphorylation expression.

Bottom Line: Inactivity is associated with a loss of muscle mass, which is also reversed with isometric exercise training.This impairment was improved by superoxide dismutase mimic Tempol.This improvement was blunted by nitric oxide (NO) synthase inhibitor l-NG-nitroarginine methyl ester (l-NAME).

View Article: PubMed Central - PubMed

Affiliation: Vascular Biology Center and Department of Physiology, Georgia Regents University, Augusta, GA, Germany (S.Q., J.D.M., C.D.S., W.H., A.G., F.C., Y.Y., Y.S., D.J.F., D.W.S.).

Show MeSH
Related in: MedlinePlus