Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/6536
Title: Bone mass and the CAG and GGN androgen receptor polymorphisms in young men
Authors: Guadalupe-Grau, Amelia
Rodriguez-Gonzalez, Francisco Germán
Ponce-González, Jesús Gustavo
Dorado, Cecilia 
Olmedillas, Hugo
Fuentes, Teresa
Pérez-Gómez, Jorge
Sanchis-Moysi, Joaquin 
Diaz-Chico, Bonifacio
Calbet, Jose A. L. 
UNESCO Clasification: 241106 Fisiología del ejercicio
Keywords: Testosterone
Bone
Osteoporosis
Androgens
Issue Date: 2010
Journal: PLoS ONE 
Abstract: BACKGROUND: To determine whether androgen receptor (AR) CAG (polyglutamine) and GGN (polyglycine) polymorphisms influence bone mineral density (BMD), osteocalcin and free serum testosterone concentration in young men. METHODOLOGY/PRINCIPAL FINDINGS: Whole body, lumbar spine and femoral bone mineral content (BMC) and BMD, Dual X-ray Absorptiometry (DXA), AR repeat polymorphisms (PCR), osteocalcin and free testosterone (ELISA) were determined in 282 healthy men (28.6+/-7.6 years). Individuals were grouped as CAG short (CAG(S)) if harboring repeat lengths of < or = 21 or CAG long (CAG(L)) if CAG > 21, and GGN was considered short (GGN(S)) or long (GGN(L)) if GGN < or = 23 or > 23. There was an inverse association between logarithm of CAG and GGN length and Ward's Triangle BMC (r = -0.15 and -0.15, P<0.05, age and height adjusted). No associations between CAG or GGN repeat length and regional BMC or BMD were observed after adjusting for age. Whole body and regional BMC and BMD values were similar in men harboring CAG(S), CAG(L), GGN(S) or GGN(L) AR repeat polymorphisms. Men harboring the combination CAG(L)+GGN(L) had 6.3 and 4.4% higher lumbar spine BMC and BMD than men with the haplotype CAG(S)+GGN(S) (both P<0.05). Femoral neck BMD was 4.8% higher in the CAG(S)+GGN(S) compared with the CAG(L)+GGN(S) men (P<0.05). CAG(S), CAG(L), GGN(S), GGN(L) men had similar osteocalcin concentration as well as the four CAG-GGN haplotypes studied. CONCLUSION: AR polymorphisms have an influence on BMC and BMD in healthy adult humans, which cannot be explained through effects in osteoblastic activity.
URI: http://hdl.handle.net/10553/6536
ISSN: 1932-6203
DOI: 10.1371/journal.pone.0011529
Source: Plos One [ISSN 1932-6203],v. 5 (7)
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