| pubmed-article:21084444 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21084444 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:21084444 | lifeskim:mentions | umls-concept:C0026845 | lld:lifeskim |
| pubmed-article:21084444 | lifeskim:mentions | umls-concept:C0039601 | lld:lifeskim |
| pubmed-article:21084444 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:21084444 | lifeskim:mentions | umls-concept:C0021665 | lld:lifeskim |
| pubmed-article:21084444 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
| pubmed-article:21084444 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:21084444 | pubmed:dateCreated | 2010-12-24 | lld:pubmed |
| pubmed-article:21084444 | pubmed:abstractText | Testosterone (T) supplementation increases skeletal muscle mass, circulating GH, IGF-I, and im IGF-I expression, but the role of GH and IGF-I in mediating T's effects on the skeletal muscle remains poorly understood. Here, we show that T administration increased body weight and the mass of the androgen-dependent levator ani muscle in hypophysectomized as well as castrated plus hypophysectomized adult male rats. T stimulated the proliferation of primary human skeletal muscle cells (hSKMCs) in vitro, an effect blocked by transfecting hSKMCs with small interference RNA targeting human IGF-I receptor (IGF-IR). In differentiation conditions, T promoted the fusion of hSKMCs into larger myotubes, an effect attenuated by small interference RNA targeting human IGF-IR. Notably, MKR mice, which express a dominant negative form of the IGF-IR in skeletal muscle fibers, treated with a GnRH antagonist (acyline) to suppress endogenous T, responded to T administration by an attenuated increase in the levator ani muscle mass. In conclusion, circulating GH and IGF-I are not essential for mediating T's effects on an androgen-responsive skeletal muscle. IGF-I signaling plays an important role in mediating T's effects on skeletal muscle progenitor cell growth and differentiation in vitro. However, IGF-IR signaling in skeletal muscle fibers does not appear to be obligatory for mediating the anabolic effects of T on the mass of androgen-responsive skeletal muscles in mice. | lld:pubmed |
| pubmed-article:21084444 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21084444 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21084444 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21084444 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21084444 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21084444 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21084444 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:21084444 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21084444 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21084444 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21084444 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21084444 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21084444 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21084444 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:21084444 | pubmed:issn | 1945-7170 | lld:pubmed |
| pubmed-article:21084444 | pubmed:author | pubmed-author:JasujaRaviR | lld:pubmed |
| pubmed-article:21084444 | pubmed:author | pubmed-author:BhasinShalend... | lld:pubmed |
| pubmed-article:21084444 | pubmed:author | pubmed-author:BartonElisabe... | lld:pubmed |
| pubmed-article:21084444 | pubmed:author | pubmed-author:ShanskyJanetJ | lld:pubmed |
| pubmed-article:21084444 | pubmed:author | pubmed-author:VandenburghHe... | lld:pubmed |
| pubmed-article:21084444 | pubmed:author | pubmed-author:TravisonThoma... | lld:pubmed |
| pubmed-article:21084444 | pubmed:author | pubmed-author:MorrisCarlC | lld:pubmed |
| pubmed-article:21084444 | pubmed:author | pubmed-author:SerraCarloC | lld:pubmed |
| pubmed-article:21084444 | pubmed:author | pubmed-author:ZhangAnqiA | lld:pubmed |
| pubmed-article:21084444 | pubmed:author | pubmed-author:TangherliniFr... | lld:pubmed |
| pubmed-article:21084444 | pubmed:author | pubmed-author:GannoMichelle... | lld:pubmed |
| pubmed-article:21084444 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21084444 | pubmed:volume | 152 | lld:pubmed |
| pubmed-article:21084444 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21084444 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21084444 | pubmed:pagination | 193-206 | lld:pubmed |
| pubmed-article:21084444 | pubmed:dateRevised | 2011-2-7 | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:meshHeading | pubmed-meshheading:21084444... | lld:pubmed |
| pubmed-article:21084444 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21084444 | pubmed:articleTitle | The role of GH and IGF-I in mediating anabolic effects of testosterone on androgen-responsive muscle. | lld:pubmed |
| pubmed-article:21084444 | pubmed:affiliation | Section of Endocrinology, Diabetes, and Nutrition, Boston Medical Center, 670 Albany Street, Boston, Massachusetts 02118, USA. cserra@bu.edu | lld:pubmed |
| pubmed-article:21084444 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21084444 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:21084444 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
