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Effects of a CRF2R agonist and exercise on mdx and wildtype skeletal muscle
Author(s) -
Hall Julie E.,
Kaczor Jan J.,
Hettinga Bart P.,
Isfort Robert J.,
Tarnopolsky Mark A.
Publication year - 2007
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.20820
Subject(s) - endocrinology , medicine , agonist , creatine kinase , skeletal muscle , atrophy , mdx mouse , placebo , muscle atrophy , amyotrophy , receptor , dystrophin , pathology , alternative medicine
Corticotrophin‐releasing factor 2 receptor (CRF2R) agonists prevent muscle atrophy due to immobilization, denervation, and corticosteroid‐induced muscle atrophy in wildtype mice. We hypothesized that a CRF2R agonist will increase skeletal muscle mass in mdx mice. Mdx (C57BL/10ScSn‐ Dmd mdx ) and wildtype (C57BL/6) mice were divided into four groups: sedentary placebo, sedentary CRF2R agonist, exercised placebo, and exercised CRF2R agonist. Mice exercised on a treadmill twice weekly for 30 min (8–12 m/min, 8 weeks). Muscle and heart weights, serum creatine kinase, and γ‐glutamyltransferase activities were measured. The CRF2R agonist increased extensor digitorum longus and soleus muscle weights ( P < 0.05) in wildtype and mdx mice. Sedentary mdx CRF2R and exercised mdx placebo mice had lower serum creatine kinase activity than sedentary mdx placebo mice. CRF2R‐treated mice had decreased heart weights compared to placebo‐treated mice. We conclude that CRF2R agonists should be further evaluated as a potential therapy for dystrophinopathies. Muscle Nerve, 2007