期刊
BRAIN RESEARCH
卷 1364, 期 -, 页码 186-197出版社
ELSEVIER
DOI: 10.1016/j.brainres.2010.08.088
关键词
Obesity; Hyperandrogenism; Luteinizing hormone; Puberty; Polycystic ovary syndrome
资金
- Eunice Kennedy Shriver NICHD/NIH [U54 041859]
- National Center For Research Resources [HD 39267, RR-00055, UL1RR024999]
Optimal fat mass is necessary for normal gonadotropin levels in adults, and both undernutrition and overnutrition suppress gonadotropins thus the gonadotropin response to relative adipose mass is biphasic Adult obesity is associated with blunted luteinizing hormone (LH) pulse amplitude that is partially attributable to increased LH clearance rate Testosterone appears to have a biphasic effect on gonadotropin production in females Moderate elevations of testosterone appear to stimulate LH production at both the hypothalamic and pituitary level while very high levels of testosterone suppress LH Thus obesity per se appears to suppress gonadotropin production and moderate hyperandrogenemia in women appears to stimulate LH The ordinary hypergonadotropic hyperandrogenism of obese women appears to be an exception to this model because it is usually due to polycystic ovary syndrome (PCOS) a condition in which intrinsic functional ovarian hyperandrogenism and excess adiposity share a common origin that involves insulin resistant hyperinsulinemia LH elevation seems to be secondary to hyperandrogenemia and is absent in the most obese cases Overweight early pubertal girls have significant blunting of sleep related LH production which is the first hormonal change of puberty The data are compatible with the possibility that excess adiposity may paradoxically subtly suppress hypothalamic-pituitary-gonadal function in early puberty although it is known to contribute to the early onset of puberty (C) 2010 Elsevier B V All rights reserved
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据