卵泡刺激素介导睾酮诱导的精子发生抑制的差异

睾酮 (T)诱导的精子发生抑制是男性激素避孕的理论基础 ,但该方法不能使所有受试者达到无精子 ,部分受试者维持低水平的精子发生。睾内T水平在无精子组与少精子组之间没有差异 ,5α还原酶和双氢睾酮 (DHT)的作用至今未得到证实。大量的实验和部分临床研究表明 ,卵泡刺激素 (FSH)可能是低促性腺激素和低睾内T状态下维持一定水平精子发生的重要因素 ,其机制可能是刺激亮A型精原细胞 (Ap)增加和Ap→B型精原细胞的转化 ,以及介导精子排放。但也有完全不同的研究结果 ,人与动物和人种之间也存在差异     

FSH及其受体基因多态性与男性精子发生相关性

卵泡刺激素(FSH)是一种由脑垂体合成并分泌的激素,与支持细胞膜上的FSH受体(FSHR)结合,提高支持细胞合成雄激素结合蛋白的水平,同时分泌抑制素,在生精过程中起到至关重要的作用。随着DNA测序技术的发展,检测到FSH基因单核苷酸多态性(SNP)rs10835638和FSHR基因SNPs rs6165,rs6166,rs1394205,这些SNPs可能直接影响FSH表达水平和FSHR的活性,在男性主要表现为精子发生障碍。本文综述FSH及FSHR基因多态性与男性精子发生的相关性。     

男科病人内分泌激素放免测定意义初探

目的：探讨男科病人内分泌激素与不育症、性功能障碍之间的关系。方法：采用放免法（ＲＩＡ）对正常组２０例、不育症组６８例、性功能障碍组４２例进行卵泡刺激（ＦＳＨ）、黄体生成素（ＬＨ）、催乳素（ＰＲＬ）睾酮（Ｔ＿雌二醇（Ｅ２）的测定。采用方差分析和两两对比进行实验结果分析，结果：Ｔ于正常组与不育症组有非常显著差异，不育症组与性功能障碍组差异显著。ＦＳＨ于不 育?     

精子发生的内分泌激素调节

下丘脑-垂体-睾丸轴系对男性生殖功能起着关键性作用,精子发生是这个轴系精密调节的结果。下丘脑促性腺激素释放激素(GnRH)脉冲式释放控制了卵泡刺激素(FSH)和黄体生成素(LH)的波动性分泌,GnRH脉冲频率的变化调节垂体促性腺细胞分泌两种不同的激素,是一种独具一格的机制。促性腺激素抑制激素(GnIH)于2000年首次从鹌鹑垂体鉴定出来。GnIH的发现使我们更深入地了解下丘脑激素对垂体促性腺细胞的调节。哺乳动物的GnIH神经元定位于下丘脑背内侧核,轴突延伸至正中隆突。GnIH通过其受体GPR147抑制垂体促性腺细胞的功能。成年男子的精子发生需要FSH和睾酮的共同作用,任何二者之一缺失会损害Sertoli细胞的分化和功能以及生精细胞在精子发生过程的发育。睾酮至少从4个方面促进精子发生:(1)紧密连接(tight junction)的形成和功能;(2)附睾的发育和功能;(3)生精细胞的发育;(4)精子释放。在体研究提示,雌激素亦对精子发生起重要作用,雌二醇调节小鼠精原细胞系和精母细胞系调亡和抗调亡之间的平衡。     

男科病人内分泌激素放免测定意义初探

目的：探讨男科病人内分泌激素与不育症、性功能障碍之间的关系。方法：采用放免法（RIA）对正常组20例、不育症组68例、性功能障碍组42例进行卵泡刺激素（FSH）、黄体生成素（LH）、催乳素（PRL）、睾酮（T）、雌二醇（E2）的测定。采用方差分析和两两对比进行实验结果分析。结果：T于正常组与不育症组有非常显著差异（P＜0．01），不育症组与性功能障碍组差异显著（P＜0．05）。FSH于不育症组与性功能障碍组差异显著（P＜0．05），不育症组与正常组相差非常显著（P＜0．01）。结论：男科病人内分泌激素中T与不育症、性功能障碍关系密切，FSH与不育症关系明显。     

雄激素与精子发生的关系

雄激素被认为在精子发生中具有重要作用.近年的动物实验以及临床研究提示,雄激素可以导致严重少精子或者无精子症,内源性睾酮可以引起生精细胞凋亡,与生精细胞阻滞高度相关.本文对近年的材料进行分析后,认为雄激素与精子发生的关系在于,雄激素可以引起生精细胞凋亡,造成细胞重排,对精子发生起到调节作用.     

促性腺激素的同分异构体

卵巢的反应性受多种因素的影响,高龄、卵巢手术、盆腔结核、盆腔炎症、免疫性因素等均可导致卵巢低反应.近年来发现卵泡刺激素(FSH)的同分异构体、FSH受体基因突变及多态性导致FSH受体结构和功能异常,也是卵巢反应异常的原因之一[1].在促排卵过程中,应综合考量可能影响卵巢反应性的各种因素,尤其是FSH异构体的不同生物学特性导致的卵巢反应差异,选择合适的促排卵方案,达到相对较为满意的结局.     

激素对精子发生的调控

精子发生是一个连续不断的细胞增生与分化的过程 ,是激素依赖的调控 ,其中卵泡刺激素 (FSH)和黄体生成素 (LH)刺激释放的睾酮 (T)是主要的激素调节者。睾丸内T是维持精子发生最关健的因素之一 ,而FSH对正常精子发生的起始和维持同样是必须的。在介导激素调节中 ,Sertoli细胞处于核心地位。同时 ,正常精子发生过程中的生精细胞凋亡也是激素调控的。深入研究精子发生的激素调控 ,为探索安全、可复的男性避孕方法奠定了基础。     

烧伤对垂体—睾丸轴影响的临床研究

OBJECTIVE: To investigate the effects of burn trauma on pituitary-testis axis. METHODS: The changes in serum estradiol(E2), testosterone(T), luteinizing hormone(LH), and follicle stimulating hormone(FSH) levels were dynamically investigated by RIA in 30 days after thermal injury in 28 burnt men. RESULTS: The serum FSH, LH, and T levels significantly decreased after injury, and there was some increase from PBD(postburn day) 14 to 30. In patients in group II and III (BSA > 30% TBSA), not all of their FSH, LH, and T levels reached the normal control on the PBD 30. Serum E2 levels were elevated after injury, then returned gradually to normal. In three patients who died, their mean T levels were significantly lower than patients who survived, but mean E2 levels were significantly higher than that of survivors. CONCLUSION: The activity of pituitary might be depressed after burn trauma. The imbalance between E2 and T might play a role in the processes of immuno-depression after injury. The changed extent of E2 and T levels was correlated to burn size. They could be sensitive indicators of burn stress.     

不育男性内分泌激素测定与精子密度相关研究

目的：探讨不育男性５项内分泌激素与精子密度的相关关系。方法：采取放免法（ＲＩＡ）对１１０例男性不育症进行卵泡刺激素（ＦＳＨ）、黄体生成素（ＬＨ）、催乳素（ＰＲＬ）、雌二醇（Ｅ２）、睾酮（Ｔ）的测定,实验值与同期检测的精子密度进行统计学相关分析。结果：＜４．６μｇ／Ｌ的Ｔ值与精子密度的等级相关系数ｒ＝０．７６０７（Ｐ＜０．００１）;＞１０Ｕ／Ｌ的ＦＳＨ、ＬＨ值与精子密度的等级相关系数分别是ｒ＝－０．５２８３（Ｐ＜０．００１）、ｒ＝－０．４５３１（Ｐ＜０．００５）。结论：低于正常的Ｔ值与精子密度呈正相关;高于正常的ＦＳＨ、ＬＨ值与精子密度呈负相关。     

Hormonal regulation of spermatogenesis

Proper functioning of the mammalian testis is dependent upon an array of hormonal messengers acting through endocrine, paracrine, and autocrine pathways. Within the testis, the primary messengers are the gonadotrophins, follicle stimulating hormone and luteinizing hormone, and the androgens. Abundant evidence indicates that the role of the gonadotrophins is to maintain proper functioning of testicular somatic cells. It is the androgens, primarily testosterone, which act through the somatic cells to regulate germ cell differentiation. Despite extensive research in this area, little is known about the cell-specific requirements for androgens and even less is understood about the downstream effectors of androgen signalling. However, recent work using cell-specific ablation of androgen receptor function has demonstrated a clear requirement for androgen signalling at multiple, discrete time points during spermatogenesis. These models also provide useful tools for identifying the targets of androgen receptor activity. The purpose of this review is to provide a brief overview of recent advances in our understanding of hormonal regulation of spermatogenesis, with an emphasis on the role of testosterone within the testis, and to pose important questions for future research in this field.     

Paracrine factors and the regulation of spermatogenesis

Summary Main problem: Although the gonadotropins and testosterone are required for normal spermatogenesis, it is believed that local control factors regulate spermatogenesis. For many years these regulatory factors had not been identified. Over the past five years, a number of growth factors have been identified in testis or isolated testicular cell types or secretions. Growth factors are key regulatory molecules which affect cell proliferation, meiosis, and differentiated function. These factors usually act in an autocrine (acting upon the cell which secreted it) or paracine (affecting another cell) manner and thus are involved in intercellular communications. Methods: Growth factor secretion by testicular cell types or testis tissue has been analyzed using a variety of assays measuring cell proliferation in vitro, as well as assays using immunocytochemicals. Growth factor gene expression in testis has been analyzed by Northern blot analysis and in situ hybridization, which gives information concerning the stage and cell specific expression of the gene. Inbred strains of mice with mutations or deletions in a growth factor gene has been used to suggest the function of two specific factors in testicular development and growth. Results: Among the growth factors expressed or secreted by testicular cell types, most are common to some other cell types in the body, such as transforming growth factors alpha and beta, epidermal growth factor, fibroblast-like growth factors, insulin-like growth factors, interleukins, endorphins, inhibin and activin, while others may be more testis specific such as mullerian inhibiting substance (anti-mullerian hormone) and Sertoli cell secreted growth factor. A variety of proto-oncogenes are expressed at discrete stages of spermatogenesis, as well as by the somatic cells of the testis. Many of these encode growth factors, receptors or other proteins involved in signal transduction. Conclusion: With the exception of the kit ligand and the c-kit proto-oncogene, which have been demonstrated to play a role in the survival of the primordial germ cell in the testis during embryogenesis, little is known of the direct role of the other growth factors in spermatogenesis. It is likely that in the near future that the function of many of these proteins in the regulation of spermatogenesis will be identified. Eventually, this information will be used to develop specific therapies and diagnostic procedures for the infertile male.Supported in part by NIH grant DK37919 (to D.J.L.) and a grant from the Methodist Hospital (to D.J.L.) The senior author (C.S.N.) is an American Foundation to Urologic Diseases Scholar and a Serono/American Fertility Society Fellow     

Hormonal regulation of mammary differentiation and milk secretion

The endocrine system coordinates development of the mammary gland with reproductive development and the demand of the offspring for milk. Three categories of hormones are involved. The levels of the reproductive hormones, estrogen, progesterone, placental lactogen, prolactin, and oxytocin, change during reproductive development or function and act directly on the mammary gland to bring about developmental changes or coordinate milk delivery to the offspring. Metabolic hormones, whose main role is to regulate metabolic responses to nutrient intake or stress, often have direct effects on the mammary gland as well. The important hormones in this regard are growth hormone, corticosteroids, thyroid hormone, and insulin. A third category of hormones has recently been recognized, mammary hormones. It currently includes growth hormone, prolactin, PTHrP, and leptin. Because a full-term pregnancy in early life is associated with a reduction in breast carcinogenesis, an understanding of the mechanisms by which these hormones bring about secretory differentiation may offer clues to the prevention of breast cancer.     

Possible involvement of proteases in the regulation of spermatogenesis

Summary.  Proteolytic enzymes, which are synthesized and secreted by cells of the seminiferous tubule of the testis, have important functions in spermatogenesis. We performed metabolic studies using small peptide hormones as a substrate to investigate the activity of proteases in cultured Sertoli cells of the rat. High-performance liquid chromatographic analysis of the cell culture supernatants showed cleavage of met- and leu-enkephalin, substance P, and bradykinin. No peptidolysis was observed for the cyclic peptide oxytocin. The hormone cleavage pattern and the use of specific protease inhibitors in peptide degradation experiments demonstrated activities of several proteases in Sertoli cells. These are mainly metalloproteinases including neutral metalloendo-peptidases, angiotensin-converting enzyme and aminopeptidases. In addition, activities of serine and aspartic proteases were detected. Only marginal proteolytic activities were observed in Sertoli cell conditioned supernatants, indicating that the investigated proteases are mainly located on Sertoli cell membranes. The peptide hormones used in this study have been found to play a potential role in the endocrine, paracrine or autocrine regulation of testicular cells. The membrane-associated proteases reported here may therefore be involved in the metabolism and inactivation of these peptides.     

Hormonal control of metabolism: regulation of plasma glucose

The control of plasma glucose needs to be tightly monitored because hyperglycaemia and hypoglycaemia can lead to severe clinical problems, including death. In this article the major mechanism for the transport of glucose into and out of the blood and how that mechanism is used to monitor the circulating concentrations of glucose are discussed. A number of hormones regulate glucose in response to changes in plasma concentrations. Insulin promotes the removal of glucose and its conversion to glycogen. Glucagon, in response to falling glucose concentrations, increases the breakdown of glycogen and the release of glucose from the liver. There are many other hormones that play a part in assisting the functions of insulin and glucagon. Failures in the appropriate production of such hormones may lead to the unregulated changes in plasma glucose and subsequent health problems.     

Hormonal control of metabolism: regulation of plasma glucose

Blood glucose concentrations are required to be maintained within a narrow therapeutic range in order to ensure the normal functioning of the body. This is accomplished through a complex, interactive, finely coordinated neuro-endocrine regulatory process. Hormonal control through the opposing actions of insulin and glucagon secreted by the islet cells of the pancreas serve as the primary response mechanism to avert post-prandial hyperglycaemia and fasting hypoglycaemia. In addition to this basic response, a range of endocrine mediators concurrently intervene, to enable the fine modulation of the process through a range of insulin-dependent and insulin-independent processes, which ultimately achieve glycaemic control by influencing tissue glucose uptake, glycolysis, glycogenesis, glycogenolysis and gluconeogenesis. More recent evidence supports a central, predominantly hypothalamic role initiated through nutrient (glucose, fatty acid) and hormonal (insulin, leptin, glucagon-like peptide-1) stimuli that influences glucose regulation by direct or indirect effects on skeletal muscle glucose uptake, islet cell insulin/glucagon secretion and hepatic glucose production.     

Hormonal control of metabolism: regulation of plasma glucose

Blood glucose concentrations are required to be maintained within a narrow therapeutic range in order to ensure the normal functioning of the body. This is accomplished through a complex, interactive, finely coordinated neuro-endocrine regulatory process. Hormonal control through the opposing actions of insulin and glucagon secreted by the islet cells of the pancreas serve as the primary response mechanism to avert post-prandial hyperglycaemia and fasting hypoglycaemia. In addition to this basic response, a range of endocrine mediators concurrently intervene, to enable the fine modulation of the process through a range of insulin-dependent and insulin-independent processes, which ultimately achieve glycaemic control by influencing tissue glucose uptake, glycolysis, glycogenesis, glycogenolysis and gluconeogenesis. More recent evidence supports a central, predominantly hypothalamic role initiated through nutrient (glucose, fatty acid) and hormonal (insulin, leptin, glucagon-like peptide-1) stimuli that influences glucose regulation by direct or indirect effects on skeletal muscle glucose uptake, islet cell insulin/glucagon secretion and hepatic glucose production.     

Hormonal regulation of specific proteins in the rat epididymis

In the adult caput epididymidis, three specific prealbumin proteins (B2, B3, and B4) could be visualized by polyacrylamide gel electrophoresis. Castration caused the disappearance of B2 and B4, and B3 became faint. Androgen administration to castrated rat restored the protein pattern to normal. In the cauda epididymidis of the control rat, four prealbumin proteins (B1-B4) were seen of which only B3 was evident after castration. The dose of androgen administered was insufficient to restore the protein pattern of the cauda epididymidis. The caput epididymidis thus appears to have a lower androgen requirement than the cauda in regard to its protein pattern.