2000
DOI: 10.1016/s0015-0282(99)00634-2
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Androgen excess contributes to altered growth hormone/insulin-like growth factor-1 axis in nonobese women with polycystic ovary syndrome

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Cited by 22 publications
(9 citation statements)
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“…In this study, serum IGF-I concentration was increased in women with PCOS compared with controls but was not related to sympathetic nerve traffic. The elevated serum IGF-I levels in the present study are in line with a previous observation in lean PCOS women, whereas obese PCOS women exhibited normal levels (32,53), indicating that it is the androgen excess that contributes to the elevated IGF-I levels.…”
Section: Discussionsupporting
confidence: 92%
See 1 more Smart Citation
“…In this study, serum IGF-I concentration was increased in women with PCOS compared with controls but was not related to sympathetic nerve traffic. The elevated serum IGF-I levels in the present study are in line with a previous observation in lean PCOS women, whereas obese PCOS women exhibited normal levels (32,53), indicating that it is the androgen excess that contributes to the elevated IGF-I levels.…”
Section: Discussionsupporting
confidence: 92%
“…Nonetheless, PCOS is associated with hyperandrogenemia, hyperinsulinemia, and insulin resistance, as well as abdominal obesity and cardiovascular disease, all factors hypothesized to be associated with increased activity of the sympathetic nervous system (8). Furthermore, PCOS is associated with disturbances in the somatotropic axis, i.e., the growth hormone (GH)/insulin growth factor (IGF)-I axis (53), which plays a central role in the regulation of central sympathetic outflow (42)(43)(44).…”
mentioning
confidence: 99%
“…Both are further affected by some neurotransmitters like dopamine and opioids (Muller et al 1999). In PCOS, the dopaminergic activity is found to be reduced (Paradisi et al 1988) and thus can affect the GH level (Wu et al 2000). The GH exerts most of its function through peripheral IGF-1 (Adashi et al 1985, Katz et al 1993, which in turn participates in the negative feedback regulation of GH (Katz et al 1993, Muller et al 1999.…”
Section: Pcos and Growth Hormonementioning
confidence: 99%
“…The GH exerts most of its function through peripheral IGF-1 (Adashi et al 1985, Katz et al 1993, which in turn participates in the negative feedback regulation of GH (Katz et al 1993, Muller et al 1999. The hyperinsulinemia seen in PCOS can increase free IGF-1 production which in turn can decrease GH release through increased hypothalamic somatostatin secretion (Wu et al 2000). Somatostatin release can also be directly stimulated by hyperandrogenemia as testosterone can increase somatostatin secretion.…”
Section: Pcos and Growth Hormonementioning
confidence: 99%
“…Altered FSHR function caused by a number of FSHR genetic variants induces arrest of follicle development, resulting in functional changes, such as primary amenorrhea, hypoplastic ovary, and high FSH serum levels. Altered FSH/LH ratio was linked with insulin resistance [15], and with altered production of and responsiveness to sex hormones, in particular testosterone [16].…”
Section: Introductionmentioning
confidence: 99%