A long-held belief is that pituitary hormones bind to their cognate receptors in classical target glands to actuate their manifold functions. However, a number of studies have shown that multiple types of pituitary hormone receptors are widely expressed in non-classical target organs. Each pituitary gland-derived hormone exhibits a wide range of nonconventional biological effects in these non-classical target organs. Herein, the extra biological functions of pituitary hormones, thyroid-stimulating hormone, follicle-stimulating hormone, luteinizing hormone, adrenocorticotrophic hormone, and prolactin when they act on non-classical organs were summarized, defined by the novel concept of an "atypical pituitary hormone-target tissue axis." This novel proposal explains the pathomechanisms of abnormal glucose and lipid metabolism, obesity, hypertension, fatty liver, and atherosclerosis while offering a more comprehensive and systematic insights into the coordinated regulation of environmental factors, genetic factors, and neuroendocrine hormones on human biological functions. The continued exploration of the physiology of the "atypical pituitary hormone-target tissue axis" could enable the identification of novel therapeutic targets for metabolic diseases.
Humans ; Pituitary Hormones/metabolism* ; Luteinizing Hormone ; Follicle Stimulating Hormone ; Prolactin ; Pituitary Gland/metabolism*

Primary ovarian insuffiency (POI), which accounts for female infertility, is characterized by amenorrhea before the age of 40 and high serum level of follicular stimulating hormone (>40 U/L) at two measurements taken at least one month apart. The disorder is believed to have a strong genetic component. A large number of candidate genes have been proposed, though few of them were extensively studied. With the rapid evolvement of genome sequencing technology, recent research raised the possibility that the genes involved in essential steps of meiosis such as chromosome synapsis and recombination play an important role in the pathogenesis of POI. Clarifying the genetic pathogenesis of POI not only can enhance understanding of the molecular mechanism of reproductive functions and infertility, but also provide accurate information for genetic counseling for such patients.
Female ; Follicle Stimulating Hormone ; metabolism ; Humans ; Infertility, Female ; genetics ; Meiosis ; Primary Ovarian Insufficiency ; genetics ; metabolism

Apoptosis of spermatogenic cells is an important physiological mechanism that keeps spermatogenesis homeostatic and restricts germ cells amount in seminiferous epithelium and is regulated and controlled by multi-factors. This article summarized recent studies on regulation of cells apoptosis by hormone, genes and various physical and chemical factors in spermatogenesis.
Animals ; Apoptosis ; genetics ; Follicle Stimulating Hormone ; metabolism ; Gene Expression Regulation ; Humans ; Male ; Spermatogenesis ; genetics

OBJECTIVESTo measure continuously the urine beta-FSH excretion in the patients with male hypogonadism, and to evaluate the significance of urine beta-FSH when used in the clinical practice and pathophysiological study on male hypogonadism.

METHODSFour health male volunteers (aged 19, 22, 27 and 33 years), four patients with the hypogonadotropic hypogonadism (aged 17, 17, 19 and 24 years) and five patients with idiopathy hypogonadism (hypergonadotropic, aged 16, 16, 17, 20 and 22 years) were asked to collect their morning-first urine samples for 30 to 32 days. One normal men collected his urine samples for 63 days. The urine beta-FSH was assayed with the method of EIA, then corrected by creatinine (Cr) concentration.

RESULTSThe urine beta-FSH level of normal men was (1.16 +/- 0.20) micrograms/mg Cr, with the peak variation in their curves, peak level at 2.76 micrograms/mg Cr. The levels of urine beta-FSH of 4 patients with the hypogonadotropic hypogonadism were lower significantly than those of normal men [(0.58 +/- 0.31) (0.93 +/- 0.47) (0.47 +/- 0.33) and (0.60 +/- 0.40) micrograms/mg Cr], without fluctuation in their curves. beta-FSH levels of 5 patients with idiopathy hypogonadism were higher significantly [(3.02 +/- 0.93), (4.36 +/- 1.12), (4.79 +/- 0.78), (4.64 +/- 1.42) and (3.88 +/- 1.42) micrograms/mg Cr], with irregular fluctuation, the highest peak level at 6.83 micrograms/mg Cr. The second sexual characteristics of hypogonadal patients were poor and serum testosterone levels low.

CONCLUSIONSThe urine beta-FSH level raised with irregular fluctuation in patients with idiopathy hypogonadism, while lowed without any fluctuation in patients with the hypogonadism. These findings suggested that the urine beta-FSH excretion was useful for the clinically classified diagnoses and pathophysiological study on male hypogonadism, and for observing the treatment reaction of androgen replacement.

Adolescent ; Adult ; Follicle Stimulating Hormone, beta Subunit ; urine ; Humans ; Hypogonadism ; metabolism ; urine ; Luteinizing Hormone ; urine ; Male ; Testosterone ; urine

Anti-Müllerian hormone (AMH) is a functional marker of fetal Sertoli cells. The germ cell number in adults depends on the number of Sertoli cells produced during perinatal development. Recently, AMH has received increasing attention in research of disorders related to male fertility. This paper reviews and summarizes the articles on the regulation of AMH in males and the serum levels of AMH in male fertility-related disorders. We have determined that follicle-stimulating hormone (FSH) promotes AMH transcription in the absence of androgen signaling. Testosterone inhibits the transcriptional activation of AMH. The undetectable levels of serum AMH and testosterone levels indicate a lack of functional testicular tissue, for example, that in patients with anorchia or severe Klinefelter syndrome suffering from impaired spermatogenesis. The normal serum testosterone level and undetectable AMH are highly suggestive of persistent Müllerian duct syndrome (PMDS), combined with clinical manifestations. The levels of both AMH and testosterone are always subnormal in patients with mixed disorders of sex development (DSD). Mixed DSD is an early-onset complete type of disorder with fetal hypogonadism resulting from the dysfunction of both Leydig and Sertoli cells. Serum AMH levels are varying in patients with male fertility-related disorders, including pubertal delay, severe congenital hypogonadotropic hypogonadism, nonobstructive azoospermia, Klinefelter syndrome, varicocele, McCune-Albright syndrome, and male senescence.
Anti-Mullerian Hormone/metabolism* ; Follicle Stimulating Hormone/blood* ; Gene Expression Regulation ; Humans ; Infertility, Male/blood* ; Male ; Testosterone/blood*

OBJECTIVETo evaluate the effects of improved experimental left varicocele (ELV) on follicle-stimulating hormone (FSH) and inhibin B (InhB).

METHODSELV models were established by the improved method in 30 SD rats, and another 30 were included in a sham operation group as controls. Three months after the operation, the concentrations of the FSH and InhB were assayed by ELISA.

RESULTSThe concentration of FSH in the serum was significantly higher in the experimental group ([37.56 +/- 9.72] ng/ml) than in the control ([26.69 +/- 5.33] ng/ml) (P < 0.05), while that of InhB significantly lower in the former ([349.93 +/- 99.48] pg/ml) than in the latter ([768. 83 +/- 146.96] pg/ml) (P < 0.05).

CONCLUSIONImproved ELV can increase FSH and reduce InhB in rats, which may be associated with subfertility.

Animals ; Disease Models, Animal ; Follicle Stimulating Hormone ; metabolism ; Inhibins ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Varicocele ; metabolism

OBJECTIVESTo investigate the tissue ultrastructure changes of small testis and sex hormone and their correlation.

METHODSThe patients were divided into small tests (n = 8) and control group(n = 12). FSH, LH, T were determined by radioimmunassay. Diameter and wall thickness of convoluted seminiferous tubule were investigated with light microscope and electro microscopy on small testis tissue morphology and ultrastructure.

RESULTSFSH, LH, T of small testis and control group were (21.05 +/- 9.15) IU/L vs (6.74 +/- 3.52) IU/L, (22.88 +/- 6.25) IU/L vs (6.60 +/- 1.48) IU/L and (0.30 +/- 0.04) nmol/L vs (17.55 +/- 9.25) nmol/L, respectively. Seminiferous tubule diameter and wall thickness were(37.33 +/- 6.80) microns vs (198.46 +/- 29.84) microns and (10.30 +/- 1.82) microns vs (2.95 +/- 0.20) microns. Small testis tissue ultrastructure changed significantly.

CONCLUSIONSPathologic changes of small testis tissue in many parts such as seminiferous tubule, germinal epithelium, Sertoli cell, Leydig cell, limiting membrance and blood vessel may relate with genetics and immunoreaction.

Adult ; Follicle Stimulating Hormone ; metabolism ; Gonadal Steroid Hormones ; metabolism ; Humans ; Luteinizing Hormone ; metabolism ; Male ; Statistics as Topic ; Testis ; anatomy & histology ; metabolism ; ultrastructure ; Testosterone ; metabolism

Alzheimer's disease (AD) is the most common type of dementia. Almost two-thirds of patients with AD are female. The reason for the higher susceptibility to AD onset in women is unclear. However, hormone changes during the menopausal transition are known to be associated with AD. Most recently, we reported that follicle-stimulating hormone (FSH) promotes AD pathology and enhances cognitive dysfunctions via activating the CCAAT-enhancer-binding protein (C/EBPβ)/asparagine endopeptidase (AEP) pathway. This review summarizes our current understanding of the crucial role of the C/EBPβ/AEP pathway in driving AD pathogenesis by cleaving multiple critical AD players, including APP and Tau, explaining the roles and the mechanisms of FSH in increasing the susceptibility to AD in postmenopausal females. The FSH-C/EBPβ/AEP pathway may serve as a novel therapeutic target for the treatment of AD.
Female ; Humans ; Male ; Alzheimer Disease/pathology* ; CCAAT-Enhancer-Binding Protein-beta/metabolism* ; Cognitive Dysfunction/metabolism* ; Signal Transduction ; Follicle Stimulating Hormone

OBJECTIVETo evaluate the androgenic and anti-androgenic effects of GH (growth hormone) transgenic carp in male rats.

METHODSHershberger assay was carried out in castrated male SD rats aged 4-5 weeks. Testosterone propionate (TP) (0.4 mg/kg BW) was administrated for a positive control, GH transgenic carp (3.0 g/kg BW)+TP (0.4 mg/kg BW), parental carp (3.0 g/kg BW) + TP (0.4 mg/kg BW), and flutamide (Flu) (3.0 g/kg BW) were used for negative controls, and vehicle was administered orally for a blank control. All groups were administrated for 10 consecutive days. At the end of the test, animals were anesthetized, then weights of accessory sex organ were measured. Serum testosterone (T), luteinizing hormone (LH), and Follicle-Stimulating Hormone (FSH) levels were detected.

RESULTSThe weights ratios of the accessory sex organs and body weights showed no significant differences between the solvent control and the GH transgenic carp-treated groups. Serum concentrations of FSH, LH, and T of the rats treated with GH transgenic carp + TP showed no significant changes, compared with those treated with TP only.

CONCLUSIONGH transgenic carp does not have any androgenic agonist or antagonist properties in vivo screening tests.

Animals ; Animals, Genetically Modified ; Carps ; genetics ; Follicle Stimulating Hormone ; blood ; Genitalia, Male ; drug effects ; Growth Hormone ; genetics ; metabolism ; pharmacology ; Luteinizing Hormone ; blood ; Male ; Rats ; Testosterone ; blood

Inhibin B, a glycoprotein produced predominantly by Sertoli cells and preferentially suppressing the production and secretion of follicle-stimulating hormone (FSH) in the pituitary, is closely related to spermatogenesis. Varicocele is the abnormal dilatation and tortuosity of the pampiniform plexus veins, which may contribute to spermatogenic dysfunction and male infertility. More and more evidence has shown that the level of serum inhibin B is negatively correlated with the severity of varicocele. Determination of the inhibin B level may help assess the severity of spermatogenic dysfunction of the patient and predict the outcomes of varicocele repair and therefore has a potential application value in the diagnosis and treatment of varicocele.
Follicle Stimulating Hormone ; metabolism ; Humans ; Infertility, Male ; blood ; etiology ; Inhibins ; blood ; Male ; Sertoli Cells ; Spermatogenesis ; Varicocele ; blood