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