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. 2010 Mar 3;59(6):1312–1320. doi: 10.2337/db09-1155

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© 2010 by the American Diabetes Association.

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FIG. 6. — In HFD mice with muscle-specific PTEN deletion (MPKO), the suppression of myofiber maturation and the increase in collagen deposition were blocked. A: Hematoxylin-eosin staining revealed improved maturation of myofibers in injured tibialis anterior muscles of MPKO HFD mice (right panel) compared with results in muscles of HFD control lox/lox mice (left panel). B: MPKO improved weight gain of injured tibialis anterior muscles factored for tibia length compared with results from lox/lox HFD mice (n = 12 in each group). *P < 0.01. C: At 6 and 12 days after injury, immunostaining of the differentiation marker, desmin, increased in injured muscles of MPKO mice fed the HFD (right panel) at 6 and 12 days after injury compared with results in HFD control lox/lox mice (left panel). D: At days 12 and 21 after injury, Sirius red staining for collagen in muscles of HFD MPKO mice (right panel) revealed a significant reduction vs. results in muscles of HFD lox/lox mice (left panel). Bar graphs (lower panel) represent the fractions of injured muscle staining for collagen. n = 6. *P < 0.05. E: The ratio of p-Akt/Akt (Ser473) in muscle of lox/lox mice fed the HFD was lower than in muscle of MPKO mice (n = 6 in each group). The ratio of p-S6K1/S6K1 (Thr389) had a similar pattern (n = 6 in each group). CTX, cardiotoxin injury. (A high-quality digital representation of this figure is available in the online issue.)