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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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Passive mechanical data of all 4 groups of mice. Circumferential wall stress and circumferential wall strain were similar in all genotypes. Data are shown as mean±SEM (n>8). db/db myostatin−/− indicates mice lacking both myostatin and leptin receptor; db/db, obese leptin receptor‐deficient mice heterozygous for myostastin; lean myostatin−/−, myostatin‐ mice heterozygous for leptin receptors; lean, lean dual heterozygotes.
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fig13: Passive mechanical data of all 4 groups of mice. Circumferential wall stress and circumferential wall strain were similar in all genotypes. Data are shown as mean±SEM (n>8). db/db myostatin−/− indicates mice lacking both myostatin and leptin receptor; db/db, obese leptin receptor‐deficient mice heterozygous for myostastin; lean myostatin−/−, myostatin‐ mice heterozygous for leptin receptors; lean, lean dual heterozygotes.

Mentions: All data are reported as means±SEM, with “n” representing the number of mice used in each of the experimental groups. Concentration‐response curves from isolated mesenteric arteries (Figures 7 and 8) were computer fitted to a sigmoidal curve using nonlinear regression (Prism version 5.0; GraphPad Software Inc., San Diego, CA). Maximum vessel relaxation to agonists (Figures 7D, 10A, 11D, and 12A) was measured as a percentage of preconstriction to PE and was analyzed using a multivariable regression analysis in NCSS software (NCSS, LLC, Kaysville, UT). Figure 1A was analyzed using a 1‐way ANOVA and Tukey's multiple comparisons to test myostatin mRNA level difference among different tissues. In Figure 8A through 8D, results were ranked and a 2‐way ANOVA was performed on the ranks. There were 3‐full‐model repeated‐measures analyses. All 3 used the same 2 between factors, which were factor 1 (lean versus obese) and factor 2 (with versus without myostation). For GTT results (Figure 6), the within factor was time. For vessel response curves (Figure 7), the one within factor was different doses ranging from 10−9 to 10−4 mol/L. For the passive mechanical measurements (Figure 13), within factor was pressure. All 3 full‐model repeated‐measures ANOVA were performed using the NCSS software. All remaining experiments were analyzed using a 2‐way ANOVA with Bonferroni's multiple comparisons test. The 2 factors in the 2‐way ANOVA was factor 1 (lean versus obese) and factor 2 (with versus without myostation). Figure 8A through 8D was analyzed using nonparametric repeated measurement. For all analyses, statistical significance was accepted at P<0.05.


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)

Passive mechanical data of all 4 groups of mice. Circumferential wall stress and circumferential wall strain were similar in all genotypes. Data are shown as mean±SEM (n>8). db/db myostatin−/− indicates mice lacking both myostatin and leptin receptor; db/db, obese leptin receptor‐deficient mice heterozygous for myostastin; 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

fig13: Passive mechanical data of all 4 groups of mice. Circumferential wall stress and circumferential wall strain were similar in all genotypes. Data are shown as mean±SEM (n>8). db/db myostatin−/− indicates mice lacking both myostatin and leptin receptor; db/db, obese leptin receptor‐deficient mice heterozygous for myostastin; lean myostatin−/−, myostatin‐ mice heterozygous for leptin receptors; lean, lean dual heterozygotes.
Mentions: All data are reported as means±SEM, with “n” representing the number of mice used in each of the experimental groups. Concentration‐response curves from isolated mesenteric arteries (Figures 7 and 8) were computer fitted to a sigmoidal curve using nonlinear regression (Prism version 5.0; GraphPad Software Inc., San Diego, CA). Maximum vessel relaxation to agonists (Figures 7D, 10A, 11D, and 12A) was measured as a percentage of preconstriction to PE and was analyzed using a multivariable regression analysis in NCSS software (NCSS, LLC, Kaysville, UT). Figure 1A was analyzed using a 1‐way ANOVA and Tukey's multiple comparisons to test myostatin mRNA level difference among different tissues. In Figure 8A through 8D, results were ranked and a 2‐way ANOVA was performed on the ranks. There were 3‐full‐model repeated‐measures analyses. All 3 used the same 2 between factors, which were factor 1 (lean versus obese) and factor 2 (with versus without myostation). For GTT results (Figure 6), the within factor was time. For vessel response curves (Figure 7), the one within factor was different doses ranging from 10−9 to 10−4 mol/L. For the passive mechanical measurements (Figure 13), within factor was pressure. All 3 full‐model repeated‐measures ANOVA were performed using the NCSS software. All remaining experiments were analyzed using a 2‐way ANOVA with Bonferroni's multiple comparisons test. The 2 factors in the 2‐way ANOVA was factor 1 (lean versus obese) and factor 2 (with versus without myostation). Figure 8A through 8D was analyzed using nonparametric repeated measurement. For all analyses, statistical significance was accepted at P<0.05.

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