Inhibin B is a glycoprotein secreted by testis, consisting of two disulfide-linked subunits, an alpha-subunit and a beta B-subunit. Serum inhibin B levels are significantly negatively correlated with the serum FSH levels in males, exerting a negative feedback on FSH secretion. In males the circulating levels of inhibin B increase shortly after birth and peak at 4-12 months of age, then decrease to low levels from 3-9 year. From the onset of puberty, the levels of inhibin B gradually increase. By pubertal stage II, the adult levels of inhibin B have been reached. At stage III of puberty, a negative correlation between inhibin B and FSH levels is present and persists from stage III of puberty onward. At 20-30 year of age, the levels of inhibin B reach another peak, then gradually decline with increasing age. The men with hypospermatogenesis and spermatogenesis arrest have significantly lower levels of inhibin B than those with normal spermatogenesis. The men with Sertoli-cell-only syndrome (SCO) have extremely low levels of inhibin B. There is a closely correlation between the presence of SCO and the level of serum inhibin B. A significantly positive correlation is also observed between testis volume and inhibin B level, as well as between sperm count and inhibin B level. The inhibin B is a direct product of the seminiferous tubules, reflecting the total testicular tissue. The measurable inhibin B production in adult requires the presence of germ cells. Inhibin B is regarded as a serum marker of spermatogenesis. The determination of serum inhibin B in males can be used to assess the spermatogenesis of infertile men, to diagnose the cryptorchidism and precocious puberty, to predict the outcome of testicular sperm extraction in men with non-obstructive azoospermia, and to evaluate the damage to spermatogenesis in men after radiotherapy or chemiotherapy.
Biomarkers ; blood ; Humans ; Inhibins ; blood ; Male ; Spermatogenesis ; physiology

OBJECTIVE: The purposes of the present study were to investigate the effect of gamma-radiation on the expression of inhibin-alpha proteins and genes for inhibin alpha, betaA, and betain the ovary. METHODS: Immature mice were whole-body gamma-irradiated with 25% of a lethal dose. At time 0, 3, 6, 12, and 24 hours after the irradiation,the ovaries were collected and used for immunohistochemistry for inhibin-alpha, and RT_PCR for inhibin-alpha, betaA, and betaB. RESULTS: The expression of the immunoreactive inhibins-alpha was maintained at 12 hours post-irradiation and reduced thereafter. The expression of inhibin-alpha mRNA was significantly increased with the time after the irradiation. However there were no significant changes in the expression of betaA and betaB mRNAs. CONCLUSION: It might be thought that inhibin acts as one of the regulatory factors in the gamma-radiation-induced follicular atresia in mice
Animals ; Female ; Follicular Atresia ; Immunohistochemistry ; Inhibins* ; Mice* ; Ovary* ; RNA, Messenger

OBJECTIVE: To understand the physiologic effects and secretion pattern of inhibin A and inhibin B throughout menstrual cycle in the normal reproductive women, serum values of inhibin A and inhibin B were measured. METHODS: Inhibin A and inhibin B levels were measured in 320 serum samples from 160 normal reproductive women by solid phase sandwich ELISA. RESULTS: In the normal reproductive women, inhibin A is secreted in low serum levels until the mid- proliferative phase, begins to increase in the late proliferative phase (16.53+/-1.57 pg/ml), reaches the peak in the early secretory and mid-secretory phase (45.56+/-2.37 and 45.85+/-2.08 pg/ml), and subsequently decreases in the late secretory phase. We found that inhibin B begins to increase in the early proliferative phase (65.40+/-4.08 pg/ml), is secreted in high concentration in the proliferative phase, reaches the peak in the ovulatory phase (110.74+/-9.83 pg/ml), and thereafter declines rapidly to the lowest level in the mid-secretory phase (29.59+/-2.08 pg/ml). CONCLUSION: In conclusion, serum inhibin A levels peak during the luteal phase, indicating the greatest production by the corpus luteum and serum inhibin B levels increase during the follicular phase, indicating the greatest production by follicles in early stage of development. Inhibin A is associated with the luteal function and inhibin B, the follicular function. Both inhibins are associated with the follicular maturation and development.
Corpus Luteum ; Enzyme-Linked Immunosorbent Assay ; Female ; Follicular Phase ; Humans ; Inhibins* ; Luteal Phase ; Menstrual Cycle*

Inhibin B, a dimeric glycoprotein, is directly secreted by the testis and responses to a diversity of exogenic hormones. Serum inhibin B levels will be influenced by different factors, such as age, testis volume, the time of puberty, the time of sample collection, varied groups of people and so on. Inhibin B is directly relevant to spermatogenesis of the testis and can be viewed as a valuable marker to assess male fertility. The determination of serum inhibin B has an applicable value in diagnosing the etiology of male infertility, assessing the damage to spermatogenesis in men after radiotherapy or chemiotherapy, and evaluating therapeutic effect on cryptorchidism and varicocele. Moreover, as far as assisted reproductive technology is concerned, the investigation of serum inhibin B has a predictive value in testicular sperm extraction.
Fertility ; physiology ; Humans ; Inhibins ; analysis ; physiology ; Male ; Reproductive Techniques, Assisted ; Spermatogenesis ; physiology

OBJECTIVE: To understand the physiologic effects and secretion pattern of inhibin A and inhibin B during menstrual cycle and menopausal transition, inhibin A and inhibin B levels were measured. And to detect any changes in expression of inhibins in human ovary with age, we examined immunohistochemical staining of alpha, beta A, and beta B subunits of inhibin in ovarian tissues. This study was also designed to investigate whether or not inhibin is an early marker for menopausal transition. METHODS: Inhibin A and inhibin B levels were measured in 320 samples from normal reproductive women, in 60 from perimenopausal women, and in 20 from menopausal women by ELISA. And we examined the immunohistochemical staining of alpha, beta A, and beta B subunits of inhibin in ovarian tissues of 35 normal reproductive, 20 perimenopausal, and 5 menopausal women, respectively. RESULTS: In the normal reproductive women, inhibin A begins to increase in the late proliferative phase (16.53 +/- 1.57 pg/ml), reaches the peak in the mid-secretory phase (45.85 +/- 2.08 pg/ml), and subsequently decreases. Inhibin B begins to increase in the early proliferative phase (65.40 +/- 4.08 pg/ml), reaches the peak in the ovulatory phase (110.74 +/- 9.83 pg/ml), and thereafter declines rapidly. In the perimenopausal women, mean inhibin A serum concentration was 6.68 +/- 0.53 pg/ml during proliferative phase and 21.78 +/- 3.61 pg/ml during secretory phase, which were significantly lower than that of the same phase in the normal reproductive women (P<0.01). Mean inhibin B serum concentration was 52.16 +/- 7.46 pg/ml during proliferative phase and 22.41 +/- 6.73 pg/ml during secretory phase, which were significantly lower than that of the same phase in the normal reproductive women (P<0.01, P=0.025). In the menopausal women, both inhibin A and inhibin B were not detected. In the normal reproductive women, we observed strong immunostaining for alpha subunit in granulosa cells, theca cells, and corpus luteum. Immunostaining for beta A subunit was observed in corpus luteum, but not in growing follicles. Immunostaining for beta B subunit was observed in primary follicle, granulosa and theca cells of growing follicle, and mature follicle, but less strong than immunostaining for alpha subunit. No staining for beta B subunit was observed in the corpus luteum. In the perimenopausal women, immunostaining for inhibin subunits were observed in the same pattern as that of the normal reproductive women, but weaker. Stronger immunostaining was observed in theca cells than in granulosa cells. In the menopausal women, none of the immunostaining of inhibin subunits were observed. CONCLUSION: It is concluded that inhibin A is associated with the luteal function and inhibin B, the follicular function. The secretion of inhibins decreased rapidly in the perimenopausal transition period and were not detected in the menopausal period. Inhibin A and inhibin B are associated with the follicular maturation and development. It suggests that the inhibin A and inhibin B are good candidates as markers for perimenopausal transition.
Corpus Luteum ; Enzyme-Linked Immunosorbent Assay ; Female ; Granulosa Cells ; Humans ; Inhibins* ; Menstrual Cycle ; Ovary* ; Theca Cells

A case of Clement and Scully's type II uterine tumor resembling ovarian sex cord tumors (UTROSCT) occurring in a 21-year-old woman is presented. Grossly, a 10 cm-sized fundic myometrial tumor, which was projecting into the endometrial cavity, was excised. Histologically, most parts of tumor showed the morphology of sex cord-like differentiation, including solid anastomosing cords or tubules, solid nests, and trabeculae arranged in a plexiform pattern. The sex cord elements were studied immunohistochemically with markers of sex cord, steroid cell differentiation (inhibin, O13, and A103), or both. The tumor cells were found to be diffusely immunoreactive for O13 (MIC2, CD99) and very focally positive for inhibin. There were also constant immunoreactivity for vimentin and hormone receptors and relatively rare positivity for desmin, actin, and cytokeratin. These findings provide strong evidence for the presence of true sex cord elements, the derivation of which seems to derive from the capacity for divergent differentiation of uterine stroma. This report demonstrates immunohistochemically true sex cord differentiation in UTROSCT.
Actins ; Cell Differentiation ; Desmin ; Female ; Humans ; Inhibins ; Keratins ; Vimentin ; Young Adult*

OBJECTIVESTo investigate the possible differences in the inhibin B levels of seminal plasma and serum between fertile and infertile males and to obtain information on the relation between serum inhibin B or seminal plasma inhibin B and spermatogenesis.

METHODSSemen and blood samples were collected from fertile(n = 20), oligospermia(n = 20), asthenospermia(n = 22) and non-obstructive azoospermia(NOA) (n = 20) males at 8:00 am = 10:00 am. Semen parameters were analyzed. Levels of inhibin B in seminal plasma and serum, ACP, Fru, alpha-Glu in seminal plasma, serum levels of FSH, T, LH were determined.

RESULTSBoth levels of serum inhibin B and levels of seminal plasma inhibin B correlated significantly negatively with serum FSH(r = -0.536, P < 0.001 vs r = -0.288, P = 0.01), and statistically positively with sperm concentration(r = 0.49, P < 0.001 vs r = 0.48, P < 0.001). There was positive correlation between levels of seminal plasma inhibin B and activity of alpha-Glu in seminal plasma (r = 0.377, P = 0.001). The difference in levels of seminal plasma inhibin B was found only between fertile males or asthenospermia and NOA (P < 0.01 and P < 0.05, respectively). However, significant differences in levels of serum inhibin B were found not only between males with normal sperm concentration (including fertile males and asthenospermia) and NOA (P < 0.01), fertile males and oligospermia (P < 0.05), but also between oligospermia and NOA (P < 0.05). There was no correlation between serum inhibin B and seminal plasma inhibin B.

CONCLUSIONSBoth levels of serum inhibin B and seminal plasma inhibin B could reflect testis spermatogenesis status. Levels of seminal plasma inhibin B could also reflect the function of seminiferous duct, but the wide range of values limited its applicability.

Adult ; Humans ; Infertility, Male ; blood ; metabolism ; Inhibins ; analysis ; blood ; Male ; Semen ; chemistry ; Spermatogenesis

Adrenohepatic fusion is the union of the liver and adrenal gland with close intermingling of their respective parenchymal cells. Adrenal cortical adenoma arising in adrenohepatic fusion tissue is extremely rare, although adrenohepatic fusion itself is relatively common. Here we report a case of a 59-year-old man with a mass in the right lobe of his liver. The mass showed slight hyperattenuation during arterial phase and hypoattenuation during portal phase on dynamic computed tomography with contrast enhancement. On pathology, the mass consisted of round to polygonal cells with clear microvesicular or eosinophilic cytoplasm, arranged in nests or in a trabecular pattern. The tumor cells were positive for inhibin and melan-A, but negative for Hep Par-1. In the periphery of the mass, adrenohepatic fusion was identified between the liver and adrenal gland, and was simultaneously resected with the mass. We report this rare case, and discuss its clinical implications, especially the differential diagnosis with hepatocellular carcinoma.
Adrenal Glands ; Adrenocortical Adenoma ; Carcinoma, Hepatocellular ; Cytoplasm ; Diagnosis, Differential ; Eosinophils ; Humans ; Inhibins ; Liver ; MART-1 Antigen ; Middle Aged

OBJECTIVETo investigate the relationship between pathological alterations of spermatogenic impairment in seminiferous tubules and serum inhibin B concentration in patients with azoospermia and to verify the significance of INH B in evaluating spermatogenesis.

METHODSEighty-three cases of azoospermia underwent testicular biopsy for the purpose of diagnosis. In accordance with the pathological alterations of spermatogenesis in seminiferous tubules, the samples were divided into four groups: Sertoli cell-only syndrome (n = 21); hypospermatogenesis (n = 20); maturation arrest (n = 24) and almost normal spermatogenesis (n = 18). Serum INHB and FSH, LH, T concentrations were tested before testicular biopsy for each patient respectively.

RESULTSThe INHB levels were (20. 85 +/- 18.78) pg/ml, (67.25 +/- 40.98) pg/ml, (73.63 +/- 25.54) pg/ml and (149.48 +/- 27.92) pg/ml in the above four groups, respectively. There was no significant statistical difference in the level of serum INH B between maturation arrest and hypospermatogenesis groups (P > 0.05), and there was a very significant difference in almost normal spermatogenesis group and the other three groups, respectively (P < 0.001). There was no significant difference in the concentration of serum FSH when maturation arrest group compared with spermatogenesis group (P > 0.05), whereas between the other two groups and between each of them and maturation arrest or almost normal spermatogenesis there was a very significant difference in the level of serum FSH (P < 0.05); The concentrations of LH and T were not significantly different among the four groups (P > 0.05).

CONCLUSIONSerum INHB concentration was decreased when spermatogenesis got impaired. It dropped the most markedly in Sertoli cell-only syndrome group. INH B reflects directly the spermatogenic function in seminiferous tubules of the testis. Therefore, it could be considered valuable for spermatogenesis and potential fertility in patients with azoospermia.

Adult ; Follicle Stimulating Hormone ; blood ; Humans ; Inhibins ; blood ; Luteinizing Hormone ; blood ; Male ; Oligospermia ; blood ; pathology ; Testis ; pathology ; 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