Insulin has complex effects on cell growth,metabolism and differentiation,and these effects are mediated by a cell-surface bound receptor and eventually a cascade of intracellular signaling events.Among the several me...Insulin has complex effects on cell growth,metabolism and differentiation,and these effects are mediated by a cell-surface bound receptor and eventually a cascade of intracellular signaling events.Among the several metabolic and growth-promoting effects of insulin,insulin resistance is defined as an attenuated effect of insulin on glucose metabolism,primarily the limited export of blood glucose into skeletal muscle and adipose tissue.On the other hand,not all the signaling pathways and insulin-responsive tissues are equally affected,and some effects other than the metabolic actions of insulin are overexpressed.Ovaries and the adrenal glands are two examples of tissues remaining sensitive to insulin actions where insulin may contribute to increased androgen secretion.Polycystic ovary syndrome(PCOS)is the most common form of androgen excess disorder(AED),and its pathogenesis is closely associated with insulin resistance.Patients with idiopathic hirsutism also exhibit insulin resistance,albeit lower than patients with PCOS.Although it is not as evident as in PCOS,patients with congenital adrenal hyperplasia may have insulin resistance,which may be further exacerbated with glucocorticoid overtreatment and obesity.Among patients with severe insulin resistance syndromes,irrespective of the type of disease,hyperinsulinemia promotes ovarian androgen synthesis independently of gonadotropins.It is highly debated in whom and how insulin resistance should be diagnosed and treated among patients with AEDs,including PCOS.It is not suitable to administer an insulin sensitizer relying on only some mathematical models used for estimating insulin resistance.Instead,the treatment decision should be based on the constellation of the signs,symptoms and presence of obesity;acanthosis nigricans;and some laboratory abnormalities such as impaired glucose tolerance and impaired fasting glucose.展开更多
Hirsutism,which is characterized by excessive growth of terminal hair in a male pattern,may result from various causes including polycystic ovary syndrome(PCOS),non-classic congenital adrenal hyperplasia,adrenal or ov...Hirsutism,which is characterized by excessive growth of terminal hair in a male pattern,may result from various causes including polycystic ovary syndrome(PCOS),non-classic congenital adrenal hyperplasia,adrenal or ovarian tumors or it may be idiopathic.Idiopathic hirsutism is currently defined as hirsutism associated with normal ovulatory function,normal serum androgen levels and normal ovarian morphology,however,the pathogenesis of idiopathic hirsutism is not clear.The androgens are the main hormones to stimulate growth of body hair,therefore,there should be any form of increased androgen effect irrespective of normal serum androgen levels in any patient with hirsutism.In accordance to this scientific truth,we have previously shown that,although within normal limits,patients with idiopathic hirsutism have relatively higher serum androgen levels(relative hyperandrogenemia)in comparison to healthy subjects which let as to think that is idiopathic hirsutism really idiopathic?In addition to relative hyperandrogenemia,we have previously shown that,in comparison to healthy subjects,women with idiopathic hirsutism demonstrated higher expression of steroid sulphatase and 17-beta hydroxysteroid dehydrogenase mRNA both in the subumbilical region and arm skin,which contributes to local androgen metabolism.Those results support the idea that,in some patients,although the adrenals or ovaries do not secrete increased amount of androgens leading to hyperandrogenemia,pilocebaceous unit locally produce increased amount of androgens leading to hirsutism without ovulatory dysfunction.Upon the demonstration of relative hyperandrogenemia and possible increase in local androgen synthesis in patients with idiopathic hirsutism,we think that idiopathic hirsutism is not idiopathic and it may be named as“normoandrogenic hirsutism”.Furthermore,it may not be a different entity but may be an early stage of hyperandrogenic disorders such as PCOS.Clinically,this can be find out by following-up patients with idiopathic hirsutism prospectively.展开更多
文摘Insulin has complex effects on cell growth,metabolism and differentiation,and these effects are mediated by a cell-surface bound receptor and eventually a cascade of intracellular signaling events.Among the several metabolic and growth-promoting effects of insulin,insulin resistance is defined as an attenuated effect of insulin on glucose metabolism,primarily the limited export of blood glucose into skeletal muscle and adipose tissue.On the other hand,not all the signaling pathways and insulin-responsive tissues are equally affected,and some effects other than the metabolic actions of insulin are overexpressed.Ovaries and the adrenal glands are two examples of tissues remaining sensitive to insulin actions where insulin may contribute to increased androgen secretion.Polycystic ovary syndrome(PCOS)is the most common form of androgen excess disorder(AED),and its pathogenesis is closely associated with insulin resistance.Patients with idiopathic hirsutism also exhibit insulin resistance,albeit lower than patients with PCOS.Although it is not as evident as in PCOS,patients with congenital adrenal hyperplasia may have insulin resistance,which may be further exacerbated with glucocorticoid overtreatment and obesity.Among patients with severe insulin resistance syndromes,irrespective of the type of disease,hyperinsulinemia promotes ovarian androgen synthesis independently of gonadotropins.It is highly debated in whom and how insulin resistance should be diagnosed and treated among patients with AEDs,including PCOS.It is not suitable to administer an insulin sensitizer relying on only some mathematical models used for estimating insulin resistance.Instead,the treatment decision should be based on the constellation of the signs,symptoms and presence of obesity;acanthosis nigricans;and some laboratory abnormalities such as impaired glucose tolerance and impaired fasting glucose.
文摘Hirsutism,which is characterized by excessive growth of terminal hair in a male pattern,may result from various causes including polycystic ovary syndrome(PCOS),non-classic congenital adrenal hyperplasia,adrenal or ovarian tumors or it may be idiopathic.Idiopathic hirsutism is currently defined as hirsutism associated with normal ovulatory function,normal serum androgen levels and normal ovarian morphology,however,the pathogenesis of idiopathic hirsutism is not clear.The androgens are the main hormones to stimulate growth of body hair,therefore,there should be any form of increased androgen effect irrespective of normal serum androgen levels in any patient with hirsutism.In accordance to this scientific truth,we have previously shown that,although within normal limits,patients with idiopathic hirsutism have relatively higher serum androgen levels(relative hyperandrogenemia)in comparison to healthy subjects which let as to think that is idiopathic hirsutism really idiopathic?In addition to relative hyperandrogenemia,we have previously shown that,in comparison to healthy subjects,women with idiopathic hirsutism demonstrated higher expression of steroid sulphatase and 17-beta hydroxysteroid dehydrogenase mRNA both in the subumbilical region and arm skin,which contributes to local androgen metabolism.Those results support the idea that,in some patients,although the adrenals or ovaries do not secrete increased amount of androgens leading to hyperandrogenemia,pilocebaceous unit locally produce increased amount of androgens leading to hirsutism without ovulatory dysfunction.Upon the demonstration of relative hyperandrogenemia and possible increase in local androgen synthesis in patients with idiopathic hirsutism,we think that idiopathic hirsutism is not idiopathic and it may be named as“normoandrogenic hirsutism”.Furthermore,it may not be a different entity but may be an early stage of hyperandrogenic disorders such as PCOS.Clinically,this can be find out by following-up patients with idiopathic hirsutism prospectively.
文摘目的使孕中期雌鼠暴露于高雄激素状态,观察宫内高雄激素环境是否影响子代的行为,并探讨产生焦虑行为的可能机制及多囊卵巢综合征与情志的关系。方法 Wistar雌性大鼠,分别在孕中期颈背部皮下注射T、T+Flu、T+Tam,连续3 d,所生子代雌鼠及雄鼠长至成年作为实验对象,观察基本生长情况、行为表现,检测中枢神经系统下丘脑、海马和杏仁核中关键基因的表达情况。结果 1)T组杏仁核ARm RNA的表达低于对照组。2)与对照组相比,T组子代的海马组织中ERαm RNA的表达下降。3)在T+Flu组中,下丘脑和海马中GPER m RNA的表达比T组下降。与T组相比,GPER m RNA在T+Flu和T+Tam组杏仁核中的表达显著增加。结论通过试验发现PNA大鼠焦虑行为表现更为明显,其异常的表现是通过雄激素途径发挥作用。说明子代鼠在宫内对母鼠孕期持续的高雄激素刺激产生应激,雄激素途径对子代鼠中枢神经系统产生作用,从而影响其出生后的焦虑行为。
