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In vitro experiments have demonstrated that leptin also inhibits testosterone creation right at the testes. A amount of epidemiological scientific tests have discovered that bone mineral density in the getting older male population is positively associated with endogenous androgen levels (Murphy et al 1993 Ongphiphadhanakul et al 1995 Rucker et al 2004). Testosterone amounts in youthful men have been revealed to correlate with bone sizing, indicating a position in dedication of peak bone mass and security from long term osteoporosis (Lorentzon et al 2005). Male hypogonadism has been demonstrated to be a risk issue for hip fracture (Jackson et al 1992) and a latest analyze confirmed a high prevalence of hypogonadism in a group of male clients with common age 75 a long time presenting with minimal trauma fractures in contrast to stroke victims who acted as controls (Leifke et al 2005). Estrogen is a well known determinant of bone density in women of all ages and some investigators have uncovered serum estrogen to be a robust determinant of male bone density (Khosla et al 1998 Khosla et al 2001). Serum estrogen was also uncovered to correlate better than testosterone with peak bone mass (Khosla et al 2001) but this is in contradiction of a far more recent research displaying a detrimental correlation of estrogen with peak bone measurement (Lorentzon et al 2005). Men with aromatase deficiency (Carani et al 1997) or defunctioning estrogen receptor mutations (Smith et al 1994) have been discovered to have abnormally small bone density despite ordinary or significant testosterone stages which more emphasizes the significant affect of estrogen on male bone density.
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