Satellite cell proliferation is reduced in muscles of obese Zucker rats but restored with loading.
The obese Zucker rat (OZR) is a model of metabolic syndrome, which has lower skeletal muscle size than the lean Zucker rat (LZR). Because satellite cells are essential for postnatal muscle growth, this study was designed to determine whether reduced satellite cell proliferation contributes to reduced skeletal mass in OZR vs. LZR. Satellite cell proliferation was determined by a constant-release 5-bromo-2-deoxyuridine (BrdU) pellet that was placed subcutaneously in each animal. Satellite cell proliferation, as determined by BrdU incorporation, was significantly attenuated in control soleus and plantaris muscles of the OZR compared with that shown in the LZR. To determine whether this attenuation of satellite cell activity could be rescued in OZR muscles, soleus and gastrocnemius muscles were denervated, placing a compensatory load on the plantaris muscle. In the LZR and the OZR after 21 days of loading, increases of approximately 25% and approximately 30%, respectively, were shown in plantaris muscle wet weight compared with that shown in the contralateral control muscle. The number of BrdU-positive nuclei increased similarly in loaded plantaris muscles from LZR and OZR. Myogenin, MyoD, and Akt protein expressions were lower in control muscles of OZR than in those of the LZR, but they were all elevated to similar levels in the loaded plantaris muscles of OZR and LZR. These data indicate that metabolic syndrome may reduce satellite cell proliferation, and this may be a factor that contributes to the reduced mass in control muscles of OZR; however, satellite cell proliferation can be restored with compensatory loading in OZR.
Laboratory of Muscle Biology and Sarcopenia, Division of Exercise Physiology, West Virginia School of Medicine, Robert C. Byrd Health Science Center, West Virginia Univ., Morgantown, WV 26506-9227, USA.
Jonathan M
JM
Peterson
Randall W
RW
Bryner
Stephen E
SE
Alway
D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D001973:Bromodeoxyuridine / Q000378:metabolism; D002467:Cell Nucleus / Q000378:metabolism; D049109:Cell Proliferation; D007328:Insulin / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000473:pathology* / Q000503:physiopathology; D009121:Muscle Denervation; D018482:Muscle, Skeletal / Q000294:innervation / Q000473:pathology / Q000503:physiopathology; D017570:MyoD Protein / Q000378:metabolism; D018008:Myogenin / Q000378:metabolism; D009765:Obesity / Q000097:blood / Q000378:metabolism / Q000473:pathology; D051763:PAX7 Transcription Factor / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D011924:Rats, Zucker; D032496:Satellite Cells, Skeletal Muscle / Q000378:metabolism / Q000473:pathology*; D013979:Tibial Nerve / Q000601:surgery; D016474:Weight-Bearing / Q000502:physiology*
D051017:Apoptosis Regulatory Proteins; D001786:Blood Glucose; D007328:Insulin; D017570:MyoD Protein; C057363:MyoD1 myogenic differentiation protein; C503801:Myog protein, mouse; D018008:Myogenin; D051763:PAX7 Transcription Factor; C497322:Pax7 protein, mouse; C514862:Akt1 protein, mouse; C494922:Akt2 protein, mouse; D051057:Proto-Oncogene Proteins c-akt; D001973:Bromodeoxyuridine