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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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Deletion of myostatin reduces fat mass in lean, but not obese, mice. A, Abdominal axial T1‐weighted cross‐section of MRI scan; adipose tissue is shown in white (n=3). B, Hematoxylin and eosin (H&E) staining for visceral fat (×200); bars represent 50 μm. A and B, From left to right: lean, lean myostatin−/−, db/db, and db/db myostatin−/− (n≥8). C, Visceral fat weight of all the genotypes (n≥8). D, Quantification of representative H&E‐stained cryosections, presenting as box‐and‐whisker plots comprising minimum, median, and maximum value for adipocytes diameter (n≥8). *P<0.05; **P<0.01, lean myostatin−/− versus lean or db/db myostatin−/− versus db/db; ###P<0.001; db/db versus lean or db/db myostatin−/− versus lean myostatin−/−. Data are shown as mean±SEM. 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; MRI, magnetic resonance imaging.
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fig05: Deletion of myostatin reduces fat mass in lean, but not obese, mice. A, Abdominal axial T1‐weighted cross‐section of MRI scan; adipose tissue is shown in white (n=3). B, Hematoxylin and eosin (H&E) staining for visceral fat (×200); bars represent 50 μm. A and B, From left to right: lean, lean myostatin−/−, db/db, and db/db myostatin−/− (n≥8). C, Visceral fat weight of all the genotypes (n≥8). D, Quantification of representative H&E‐stained cryosections, presenting as box‐and‐whisker plots comprising minimum, median, and maximum value for adipocytes diameter (n≥8). *P<0.05; **P<0.01, lean myostatin−/− versus lean or db/db myostatin−/− versus db/db; ###P<0.001; db/db versus lean or db/db myostatin−/− versus lean myostatin−/−. Data are shown as mean±SEM. 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; MRI, magnetic resonance imaging.

Mentions: The effect of myostatin on fat mass was examined in a similar fashion as muscle mass. Abdominal axial T1‐weighted cross‐section of all groups of mice is shown for illustrative purposes in Figure 5A. Myostatin deletion in lean mice caused a modest reduction of adipose tissue, but it had no significant effect in obese mice, indicating that whatever drives myostatin's effect in lean mice requires functional leptin signaling. Adipose tissue size was assessed histologically with H&E‐stained cryosections (Figure 5B). Visceral adipose tissue weight from each mouse genotype is shown in Figure 5C. Quantification showed that deletion of myostatin produced modest decreases in adipose tissue of lean myostatin−/−, as shown in MRI images, but db/db myostatin−/− mice remain markedly obese. Quantification of H&E staining is shown as box and whisker plots of adipocyte size (Figure 5D). Adipocytes from fat pad of obese mice were found to be of a significantly larger size (90.92±3.26 μm) than those from lean mice (50.37±1.68 μm). Myostatin deletion decreased adipocytes size (37.45±1.17 μm) in lean mice, but it had no significant effect on obese mice adipocyte size (86.59±2.44 μm; Figure 5D). Lean myostatin−/− mice had modest reduction in plasma leptin levels versus lean mice, which is consistent with reduction of adipose tissue in lean myostatin−/− mice. In obese mice, plasma leptin levels along with body weight were markedly increased and were not significantly affected by deletion of myostatin (Table 4). As shown in Table 3, deletion of myostatin produced modest reductions in visceral organ weights, explaining why significant increases in muscle mass do not greatly increase body weight, despite persistent fat mass.


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)

Deletion of myostatin reduces fat mass in lean, but not obese, mice. A, Abdominal axial T1‐weighted cross‐section of MRI scan; adipose tissue is shown in white (n=3). B, Hematoxylin and eosin (H&E) staining for visceral fat (×200); bars represent 50 μm. A and B, From left to right: lean, lean myostatin−/−, db/db, and db/db myostatin−/− (n≥8). C, Visceral fat weight of all the genotypes (n≥8). D, Quantification of representative H&E‐stained cryosections, presenting as box‐and‐whisker plots comprising minimum, median, and maximum value for adipocytes diameter (n≥8). *P<0.05; **P<0.01, lean myostatin−/− versus lean or db/db myostatin−/− versus db/db; ###P<0.001; db/db versus lean or db/db myostatin−/− versus lean myostatin−/−. Data are shown as mean±SEM. 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; MRI, magnetic resonance imaging.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4309080&req=5

fig05: Deletion of myostatin reduces fat mass in lean, but not obese, mice. A, Abdominal axial T1‐weighted cross‐section of MRI scan; adipose tissue is shown in white (n=3). B, Hematoxylin and eosin (H&E) staining for visceral fat (×200); bars represent 50 μm. A and B, From left to right: lean, lean myostatin−/−, db/db, and db/db myostatin−/− (n≥8). C, Visceral fat weight of all the genotypes (n≥8). D, Quantification of representative H&E‐stained cryosections, presenting as box‐and‐whisker plots comprising minimum, median, and maximum value for adipocytes diameter (n≥8). *P<0.05; **P<0.01, lean myostatin−/− versus lean or db/db myostatin−/− versus db/db; ###P<0.001; db/db versus lean or db/db myostatin−/− versus lean myostatin−/−. Data are shown as mean±SEM. 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; MRI, magnetic resonance imaging.
Mentions: The effect of myostatin on fat mass was examined in a similar fashion as muscle mass. Abdominal axial T1‐weighted cross‐section of all groups of mice is shown for illustrative purposes in Figure 5A. Myostatin deletion in lean mice caused a modest reduction of adipose tissue, but it had no significant effect in obese mice, indicating that whatever drives myostatin's effect in lean mice requires functional leptin signaling. Adipose tissue size was assessed histologically with H&E‐stained cryosections (Figure 5B). Visceral adipose tissue weight from each mouse genotype is shown in Figure 5C. Quantification showed that deletion of myostatin produced modest decreases in adipose tissue of lean myostatin−/−, as shown in MRI images, but db/db myostatin−/− mice remain markedly obese. Quantification of H&E staining is shown as box and whisker plots of adipocyte size (Figure 5D). Adipocytes from fat pad of obese mice were found to be of a significantly larger size (90.92±3.26 μm) than those from lean mice (50.37±1.68 μm). Myostatin deletion decreased adipocytes size (37.45±1.17 μm) in lean mice, but it had no significant effect on obese mice adipocyte size (86.59±2.44 μm; Figure 5D). Lean myostatin−/− mice had modest reduction in plasma leptin levels versus lean mice, which is consistent with reduction of adipose tissue in lean myostatin−/− mice. In obese mice, plasma leptin levels along with body weight were markedly increased and were not significantly affected by deletion of myostatin (Table 4). As shown in Table 3, deletion of myostatin produced modest reductions in visceral organ weights, explaining why significant increases in muscle mass do not greatly increase body weight, despite persistent fat mass.

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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Related in: MedlinePlus