Search Results

You are looking at 1 - 2 of 2 items for

  • Author: Helen E MacLean x
  • Refine by access: All content x
Clear All Modify Search
Yue Chen Department of Medicine, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Yue Chen in
Google Scholar
PubMed
Close
,
Jeffrey D Zajac Department of Medicine, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Jeffrey D Zajac in
Google Scholar
PubMed
Close
, and
Helen E MacLean Department of Medicine, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Helen E MacLean in
Google Scholar
PubMed
Close

Androgen treatment can enhance the size and strength of muscle. However, the mechanisms of androgen action in skeletal muscle are poorly understood. This review discusses potential mechanisms by which androgens regulate satellite cell activation and function. Studies have demonstrated that androgen administration increases satellite cell numbers in animals and humans in a dose–dependent manner. Moreover, androgens increase androgen receptor levels in satellite cells. In vitro, the results are contradictory as to whether androgens regulate satellite cell proliferation or differentiation. IGF-I is one major target of androgen action in satellite cells. In addition, the possibility of non-genomic actions of androgens on satellite cells is discussed. In summary, this review focuses on exploring potential mechanisms through which androgens regulate satellite cells, by analyzing developments from research in this area.

Free access
Helen E MacLean Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Helen E MacLean in
Google Scholar
PubMed
Close
,
Alison J Moore Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Alison J Moore in
Google Scholar
PubMed
Close
,
Stephen A Sastra Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Stephen A Sastra in
Google Scholar
PubMed
Close
,
Howard A Morris Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Howard A Morris in
Google Scholar
PubMed
Close
,
Ali Ghasem-Zadeh Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia
Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Ali Ghasem-Zadeh in
Google Scholar
PubMed
Close
,
Kesha Rana Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Kesha Rana in
Google Scholar
PubMed
Close
,
Anna-Maree Axell Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Anna-Maree Axell in
Google Scholar
PubMed
Close
,
Amanda J Notini Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Amanda J Notini in
Google Scholar
PubMed
Close
,
David J Handelsman Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by David J Handelsman in
Google Scholar
PubMed
Close
,
Ego Seeman Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia
Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Ego Seeman in
Google Scholar
PubMed
Close
,
Jeffrey D Zajac Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Jeffrey D Zajac in
Google Scholar
PubMed
Close
, and
Rachel A Davey Department of Medicine, Hanson Institute, Department of Endocrinology, ANZAC Research Institute, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia

Search for other papers by Rachel A Davey in
Google Scholar
PubMed
Close

We used our genomic androgen receptor (AR) knockout (ARKO) mouse model, in which the AR is unable to bind DNA to: 1) document gender differences between males and females; 2) identify the genomic (DNA-binding-dependent) AR-mediated actions in males; 3) determine the contribution of genomic AR-mediated actions to these gender differences; and 4) identify physiological genomic AR-mediated actions in females. At 9 weeks of age, control males had higher body, heart and kidney mass, lower spleen mass, and longer and larger bones compared to control females. Compared to control males, ARKO males had lower body and kidney mass, higher splenic mass, and reductions in cortical and trabecular bone. Deletion of the AR in ARKO males abolished the gender differences in heart and cortical bone. Compared with control females, ARKO females had normal body weight, but 14% lower heart mass and heart weight/body weight ratio. Relative kidney mass was also reduced, and relative spleen mass was increased. ARKO females had a significant reduction in cortical bone growth and changes in trabecular architecture, although with no net change in trabecular bone volume. In conclusion, we have shown that androgens acting via the genomic AR signaling pathway mediate, at least in part, the gender differences in body mass, heart, kidney, spleen, and bone, and play a physiological role in the regulation of cardiac, kidney and splenic size, cortical bone growth, and trabecular bone architecture in females.

Free access