Department of Physiology and Biophysics, Medical Center, Stony Brook University Stony Brook, NY, USA.
Front Endocrinol (Lausanne). 2012 Jan 24;2:110. doi: 10.3389/fendo.2011.00110. eCollection 2011.
In neurons, as in a variety of other cell types, the enzyme phosphatidylinositol-3-kinase (PI3K) is a key intermediate that is common to the signaling pathways of a number of peripheral metabolic cues, including insulin and leptin, which are well known to regulate both metabolic and reproductive functions. This review article will explore the possibility that PI3K is a key integrator of metabolic and neural signals regulating gonadotropin releasing hormone (GnRH)/luteinizing hormone (LH) release and explore the hypothesis that this enzyme is pivotal in many disorders where gonadotropin release is at risk. Although the mechanisms mediating the influence of metabolism and nutrition on fertility are currently unclear, the strong association between metabolic disorders and infertility is undeniable. For example, women suffering from anorectic disorders experience amenorrhea as a consequence of malnutrition-induced impairment of LH release, and at the other extreme, obesity is also commonly co-morbid with menstrual dysfunction and infertility. Impaired hypothalamic insulin and leptin receptor signaling is thought to be at the core of reproductive disorders associated with metabolic dysfunction. While low levels of leptin and insulin characterize states of negative energy balance, prolonged nutrient excess is associated with insulin and leptin resistance. Metabolic models known to alter GnRH/LH release such as diabetes, diet-induced obesity, and caloric restriction are also accompanied by impairment of PI3K signaling in insulin and leptin sensitive tissues including the hypothalamus. However, a clear link between this signaling pathway and the control of GnRH release by peripheral metabolic cues has not been established. Investigating the role of the signaling pathways shared by metabolic cues that are critical for a normal reproductive state can help identify possible targets in the treatment of metabolic and reproductive disorders such as polycystic ovarian syndrome.
在神经元中,与许多其他细胞类型一样,酶磷脂酰肌醇-3-激酶(PI3K)是许多外周代谢信号通路的关键中间产物,包括胰岛素和瘦素,它们众所周知可以调节代谢和生殖功能。这篇综述文章将探讨 PI3K 是否是调节促性腺激素释放激素(GnRH)/黄体生成素(LH)释放的代谢和神经信号的关键整合因子,并探讨该酶在许多 GnRH 释放面临风险的疾病中至关重要的假说。尽管介导代谢和营养对生育能力影响的机制目前尚不清楚,但代谢紊乱和不育之间的强烈关联是不可否认的。例如,患有厌食症的女性由于营养不良导致 LH 释放受损而出现闭经,而在另一个极端,肥胖也常与月经功能障碍和不育症并存。人们认为,代谢功能障碍相关生殖障碍的核心是下丘脑胰岛素和瘦素受体信号转导受损。虽然低水平的瘦素和胰岛素特征是负能平衡状态,但长期营养过剩与胰岛素和瘦素抵抗有关。已知会改变 GnRH/LH 释放的代谢模型,如糖尿病、饮食诱导肥胖和热量限制,也伴随着包括下丘脑在内的胰岛素和瘦素敏感组织中 PI3K 信号的受损。然而,外周代谢信号与 GnRH 释放控制之间的这种信号通路的明确联系尚未建立。研究对正常生殖状态至关重要的代谢信号通路的作用,可以帮助确定代谢和生殖障碍(如多囊卵巢综合征)治疗的可能靶点。