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PubMed2003

Modulatory effects of leptin on leydig cell function of normal and hyperleptinemic rats.

Neonatal L-monosodium glutamate (MSG) administration in rats induces several neuroendocrine and metabolic disruptions. Leptin, the adipocyte product, modulates several neuroendocrine systems including the hypothalamic-pituitary-gonadal (HPG) axis in mammals. The aim of the present study was to determine whether MSG-induced chronic hyperleptinemia could play any relevant role in the hypogonadism developed by male rats when examined in adulthood. We found that 120-day-old MSG male rats displayed significant hyperleptinemia, hypogonadism, and undisturbed basic testis structure and spermatogenesis. In vitro studies in purified Leydig cells from normal (CTR) and MSG-damaged rats revealed that basal and human chorionic gonadotropin (hCG)-stimulated 17-hydroxy-progesterone (17-HO-P(4)), Delta(4)-androstenedione (Delta(4)A) and testosterone (T) secretions were significantly lower in MSG than in CTR cells. Exposure to murine leptin (Mleptin, 10(-8)M) significantly inhibited hCG-elicited T secretion by CTR cells after 180 min incubation. While Mleptin significantly inhibited hCG-stimulated Delta(4)A output and the Delta(4)A:17-OH-P(4) ratio of secretion, conversely, it failed to modify the ratio T:Delta(4)A release by CTR Leydig cells. Interestingly, the effects of Mleptin found on CTR Leydig cells were absent in MSG Leydig cells. Finally, endogenous hyperleptinemia was associated with a significant decrease in Leydig cell expression of Ob-Rb mRNA in MSG rats. In summary, this study demonstrates that: (1) Mleptin inhibited testicular steroidogenesis in CTR rats; (2) MSG-treated rats showed lower in vitro 17-OH-P(4), Delta(4)A and T production under basal and post-hCG stimulation conditions; (3) purified Leydig cells from MSG-treated rats displayed resistance to the inhibitory action of Mleptin on T release, and (4) endogenous leptin exerts a modulatory effect on Leydig cell Ob-Rb mRNA expression. The inhibitory effect of leptin on testicular function is thus abrogated in MSG-damaged rats. The testicular leptin-resistance developed by MSG rats seems to be due to early chronic exposure of Leydig cells to high leptin circulating levels, which in turn down-regulate testicular Ob-Rb expression. It remains to be determined whether the testicular dysfunction of MSG rats can be reversed after correction of hyperleptinemia or whether it is an irreversible effect of the hypothalamic lesion.

Analysis of Variance↗
PubMed2002

Anatomical and functional evidence for a neural hypothalamic-testicular pathway that is independent of the pituitary.

Testosterone (T) secretion is classically considered to be under the primary control of pituitary LH, itself regulated by the hypothalamic peptide LH-releasing hormone. Secretagogues present in the general circulation and/or manufactured in the testis can also alter Leydig cell activity independently of the pituitary. Finally, spanchnic innervation regulates testicular LH receptors and blood flow. In the present work, we provide evidence that, in addition, there may be a neural brain-testicular circuit that regulates T release function independently of LH release. We had recently reported that the intracerebroventricular injection of IL-1beta, corticotropin-releasing factor, or beta-adrenergic agonists significantly interfered with the T response to human chorionic gonadotropin through mechanisms that did not involve LH. Here, we show that the injection of the transganglionic retrograde tracer pseudorabies virus into the testes caused viral staining in the spinal cord, the brain stem, and the hypothalamus. This observation indicates the presence of a neural pathway between the central nervous system and the testis. We then demonstrated that spinal cord injury significantly interfered with this staining, thus supporting the hypothesis that the proposed circuit travels through the cord. Finally, we showed that spinal cord injury completely abolished the ability of intracerebroventricularly injected IL-1beta or corticotropin-releasing factor to blunt the T response to human chorionic gonadotropin, which suggests that these two secretagogues act within the brain to stimulate a neural pathway that interferes with Leydig cell function independently of the pituitary. The hitherto unsuspected brain-testicular circuit that these experiments have uncovered may play a role in pathologies, so far unexplained, that are characterized by decreased T levels despite normal LH production.

Animals↗
PubMed2002

Effects of testosterone on song, aggression, and nestling feeding behavior in male great tits, Parus major.

As outlined in the trade-off hypothesis of testosterone (T) secretion, fluctuations in T during the breeding season might reflect how males allocate their time and energy to competitive behaviors for mates and territories, associated with high T levels, and parental activities, associated with low T levels. In the present study, great tit, Parus major, males were implanted with T-filled or empty silastic capsules at the start of the breeding season and the behavior of these two male categories was compared during the entire breeding season. As a measure of competitive behavior we looked at song behavior and territorial responsiveness to a male decoy, during the three main stages of the breeding period (the egg-laying, incubation, and nestling stages). As a measure of parental care we looked at feeding behavior during the nestling stage. Our results only partly supported the trade-off hypothesis. T implants increased plasma androgen levels and enhanced spontaneous song activity and the production of aggressive vocalizations in response to a decoy. However, our results suggest that the degree of physical aggression might be less than fully coupled with T. First, approach to the decoy was not affected by the treatment. Second, although T levels are known to vary from high during egg laying to low while feeding young, control and T-treated males spent similar amounts of time close to the decoy in the three breeding stages. Our results thus suggest that vocal and physical aggression might be regulated differently in the great tit. Furthermore, in contrast with most other studies on temperate bird species but in agreement with a previous study on the great tit, T treatment did not affect male feeding rates. As the dose of T we used was lower than that typically used in other studies, we cannot at present completely exclude the possibility that the latter result reflects this lower dose of T rather than the species used.

Aggression↗
PubMed2005

The effects of growth hormone and/or testosterone in healthy elderly men: a randomized controlled trial.

CONTEXT: Declines in GH and testosterone (Te) secretion may contribute to the detrimental aging changes of elderly men. OBJECTIVE: To assess the effects of near-physiological GH with/without Te administration on lean body mass, total body fat, midthigh muscle cross-section area, muscle strength, aerobic capacity, condition-specific quality of life (Age-Related Hormone Deficiency-Dependent Quality of Life questionnaire), and generic health status (36-Item Short-Form Health Survey) of older men. DESIGN, SETTINGS, AND PARTICIPANTS: A 6-month, randomized, double-blind, placebo-controlled trial was performed on 80 healthy, community-dwelling, older men (age, 65-80 yr). INTERVENTIONS: Participants were randomized to receive 1) placebo GH or placebo Te, 2) recombinant human GH (rhGH) and placebo Te (GH), 3) Te and placebo rhGH (Te), or 4) rhGH and Te (GHTe). GH doses were titrated over 8 wk to produce IGF-I levels in the upper half of the age-specific reference range. A fixed dose of Te (5 mg) was given by transdermal patches. RESULTS: Lean body mass increased with GHTe (P = 0.008) and GH (P = 0.004), compared with placebo. Total body fat decreased with GHTe only (P = 0.02). Midthigh muscle (P = 0.006) and aerobic capacity (P < 0.001) increased only after GHTe. Muscle strength changes were variable; one of six measures significantly increased with GHTe. Significant treatment group by time interactions indicated an improved Age-Related Hormone Deficiency-Dependent Quality of Life questionnaire score (P = 0.007) in the GH and GHTe groups. Bodily pain increased with GH alone, as determined by the Short-Form Health Survey (P = 0.003). There were no major adverse effects. CONCLUSION: Coadministration of low dose GH with Te resulted in beneficial changes being observed more often than with either GH or Te alone.

Aged↗
PubMed1994

Effect of FK506 on rat Leydig cell function--in vivo and in vitro study.

FK506, a macrolide antibiotic, is a potent immunosuppressant and has a biological effect similar to that of cyclosporin A (CsA). In this study, the in vivo and in vitro effects of FK506 on rat Leydig cell function were investigated. In vivo, basal testosterone levels and secretion in response to human chorionic gonadotropin (hCG) stimulation in ACl rats treated with intramuscular (IM) injections of FK506 at a dosage of 1 or 2 mg/kg/d for 14 days were not different from those of age-matched normal controls. Testicular weights (g) from rats treated with 14 injections of 1 mg/kg/d FK506 (1.08 +/- 0.08, n = 14) were similar to weights from age-matched controls (1.04 +/- 0.08, n = 14). Similarly, Wistar (Wi) rats treated with FK506 at a dosage of 1 mg/kg/d for 2 weeks showed basal testosterone and luteinizing hormone (LH) levels and secretion in response to hCG stimulation similar to those of normal controls. Histologically, the Leydig cells and germ cells in FK506-treated animals appeared normal. In vitro, basal testosterone production and response to hCG stimulation by both ACI and Wi rat Leydig cells exposed to overnight treatment of FK506 (10 to 1,000 ng/mL) were not significantly different from those of control Leydig cells. Furthermore, the viability of the Leydig cells cultured for 3 days in FK506 was not significantly different from that of controls, and they continued to secrete testosterone at a rate similar to that of controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Modulation of rat Leydig cell steroidogenic function by di(2-ethylhexyl)phthalate.

Exposure of rodents to phthalates is associated with developmental and reproductive anomalies, and there is concern that these compounds may be causing adverse effects on human reproductive health. Testosterone (T), secreted almost exclusively by Leydig cells in the testis, is the primary steroid hormone that maintains male fertility. Leydig cell T biosynthesis is regulated by the pituitary gonadotropin LH. Herein, experiments were conducted to investigate the ability of di(2-ethylhexyl)phthalate (DEHP) to affect Leydig cell androgen biosynthesis. Pregnant dams were gavaged with 100 mg(-1) kg(-1) day(-1) DEHP from Gestation Days 12 to 21. Serum T and LH levels were significantly reduced in male offspring, compared to control, at 21 and 35 days of age. However, these inhibitory effects were no longer apparent at 90 days. In a second set of experiments, prepubertal rats, from 21 or 35 days of age, were gavaged with 0, 1, 10, 100, or 200 mg(-1) kg(-1) day(-1) DEHP for 14 days. This exposure paradigm affected Leydig cell steroidogenesis. For example, exposure of rats to 200 mg(-1) kg(-1) day(-1) DEHP caused a 77% decrease in the activity of the steroidogenic enzyme 17beta-hydroxysteroid dehydrogenase, and reduced Leydig cell T production to 50% of control. Paradoxically, extending the period of DEHP exposure to 28 days (Postnatal Days 21-48) resulted in significant increases in Leydig cell T production capacity and in serum LH levels. The no-observed-effect-level and lowest-observed-effect-level were determined to be 1 mg(-1) kg(-1) day(-1) and 10 mg(-1) kg(-1) day(-1), respectively. In contrast to observations in prepubertal rats, exposure of young adult rats by gavage to 0, 1, 10, 100, or 200 mg(-1) kg(-1) day(-1) DEHP for 28 days (Postnatal Days 62-89) induced no detectable changes in androgen biosynthesis. In conclusion, data from this study show that DEHP effects on Leydig cell steroidogenesis are influenced by the stage of development at exposure and may occur through modulation of T-biosynthetic enzyme activity and serum LH levels.

Animals↗
PubMed1997

Abnormal melatonin secretion in hypogonadal men: the effect of testosterone treatment.

OBJECTIVE: We have recently demonstrated that GnRH deficient male patients have increased nocturnal melatonin secretion, whereas hypergonadotrophic hypogonadal males have decreased melatonin levels. We were interested in determining whether testosterone (T) treatment (when T levels were well matched with pubertal control values) has an effect on melatonin secretory profiles in these patients. DESIGN: Prospective, controlled. SUBJECTS: Six male patients with idiopathic hypogonadotrophic hypogonadism (IGD), six males with hypergonadotrophic hypogonadism due to Klinefelter's syndrome (KS) and seven controls. Patients were examined before and during the administration of 250 mg testosterone enanthate/month for four months. MEASUREMENTS: Serum samples for melatonin levels were obtained every 15 minutes from 1990 to 0700 h in a controlled light-dark environment. The results of FSH, LH, T and oestradiol (E2) (determined at hourly intervals) and melatonin profiles, were compared with the pre-treatment values in each group, and with values obtained in the control group. RESULTS: All 12 patients had low pre-treatment T levels (1.4 +/- 0.7 in IGD and 2.0 +/- 0.4 in KS vs. 19.8 +/- 2.3 nmol/l in controls) and attained normal levels after four months of T treatment (19.5 +/- 7 in IGD and 22.7 +/- 3.8 nmol/l in KS). Serum LH, FSH and E2 levels (11 +/- 4 IU/l, 24 +/- 10 IU/l and 113 +/- 12 pmol/l, respectively) were still elevated in KS during T treatment as compared with values in controls (2 +/- 1 IU/l, 2 +/- 1 IU/l and 67 +/- 4 pmol/l, respectively). In IGD, serum LH (0.12 +/- 0.1 IU/l) and FSH (0.16 +/- 0.2 IU/l) levels during T treatment were suppressed. Pretreatment melatonin levels in IGD were greater than those in age-matched pubertal controls while in KS, melatonin levels were lower than values in controls. Melatonin levels were equal in all 12 hypogonadal patients and controls when T levels were well matched. Mean (+/- SD) dark-time melatonin levels decreased from 286 +/- 18 to 157 +/- 26 pmol/l in IGD and increased from 92 +/- 19 to 183 +/- 48 pmol/l in KS (vs 178 +/- 59 pmol/l in controls). The integrated melatonin values decreased in IGD (from 184 +/- 14 to 102 +/- 21 pmol/min. 1 x 10(3)) and increased in KS (from 64 +/- 13 to 123 +/- 40, vs. 116 +/- 39 pmol/min. 1 x 10(3) in controls). No correlations were found between melatonin and LH, FSH or E2 levels. CONCLUSIONS: These data indicate that male patients with GnRH deficiency have increased nocturnal melatonin secretion while in hypergonadotrophic hypogonadal males melatonin secretion is decreased. Testosterone treatment normalized melatonin concentrations in these patients. Taken together, the results suggest that GnRH, gonadotrophins and gonadal steroids modulate pineal melatonin in humans.

Adolescent↗
PubMed2003

Regulation of follicle-stimulating hormone secretion by the interactions of activin-A, dexamethasone and testosterone in anterior pituitary cell cultures of male rats.

This study was designed to evaluate the effects of glucocorticoids and gonadal steroids on the expression of inhibin/activin subunits and follistatin of the anterior pituitary and test the hypothesis that resulting changes in the local activin/inhibin/follistatin tone contribute to steroid effects on follicle stimulating hormone (FSH) production from gonadotropes. In primary cell cultures of male rat anterior pituitaries, dexamethasone (DEX) or testosterone (T) stimulated FSH secretion and FSHbeta mRNA and their effects were additive with activin-A. Follistatin (FS288) and inhibin-A antagonized the rise in FSH secretion both in the absence and presence of exogenous activin-A. Despite the similarity in their action on FSH production, DEX and T had opposite effects on follistatin mRNA levels. Follistatin mRNA levels of cultured rat anterior pituitary cells were elevated upon the addition of DEX but attenuated by T. On the other hand, both DEX and T suppressed inhibin/activin betaB mRNA levels while only DEX affected betaA mRNA. In these cells, activin-A stimulated follistatin and inhibin/activin betaB mRNA levels but had no effect on betaA. Together, DEX and activin-A caused a further increase in follistatin mRNA levels while T attenuated the effect of activin-A alone. Both steroids attenuated the effect of activin-A on betaB mRNA accumulation. These results support the possibility that DEX and T, possibly acting on different subsets of anterior pituitary cells, use distinct mechanisms to modify the local activin/inhibin/follistatin circuitry and thereby upregulate FSH production from the anterior pituitary gonadotropes.

Activins↗
PubMedDate not supplied

Transplantation of newborn rat testis under the kidney capsule of adult host as a model to study the structure and function of Leydig cells.

Newborn rat testis was transplanted under the kidney capsule of adult castrated and uncastrated male rats to develop and characterize a model system for studies on Leydig cell development. Two weeks after transplantation, the number of Leydig cells and the size of their nuclei in the transplants had increased. Secretion of testosterone was indicated by increased seminal vesicle weights and decreased pituitary LH in the castrated host animals. Pituitary FSH content increased significantly in the uncastrated animals with transplants, which suggested production of an FSH-stimulating factor. Cells with the morphologic features characteristic of fetal- and adult-type Leydig cells were observed in the transplants. The seminiferous tubules with spermatocytes, incipient lumina, and significantly larger average diameters showed more advanced development than those in the normal 2-week-old testis. By the present morphologic and functional criteria, the kidney subcapsular transplantation technique provides a suitable model for studies of fetal and adult Leydig cell development.

Animals↗
PubMed2003

Androgens and estrogens induce seasonal-like growth of song nuclei in the adult songbird brain.

In seasonally breeding songbirds, the brain regions that control song behavior undergo dramatic structural changes at the onset of each annual breeding season. As spring approaches and days get longer, gonadal testosterone (T) secretion increases and triggers the growth of several song control nuclei. T can be converted to androgenic and estrogenic metabolites by enzymes expressed in the brain. This opens the possibility that the effects of T may be mediated via the androgen receptor, the estrogen receptor, or both. To test this hypothesis, we examined the effects of two bioactive T metabolites on song nucleus growth and song behavior in adult male white-crowned sparrows. Castrated sparrows with regressed song control nuclei were implanted with silastic capsules containing either crystalline T, 5alpha-dihydrotestosterone (DHT), estradiol (E(2)), or a combination of DHT+E(2). Control animals received empty implants. Song production was highly variable within treatment groups. Only one of seven birds treated with E(2) alone was observed singing, whereas a majority of birds with T or DHT sang. After 37 days of exposure to sex steroids, we measured the volumes of the forebrain song nucleus HVc, the robust nucleus of the archistriatum (RA), and a basal ganglia homolog (area X). All three steroid treatments increased the volumes of these three song nuclei when compared to blank-implanted controls. These data demonstrate that androgen and estrogen receptor binding are sufficient to trigger seasonal song nucleus growth. These data also suggest that T's effects on seasonal song nucleus growth may depend, in part, upon enzymatic conversion of T to bioactive metabolites.

Androgens↗
PubMed2002

Dehydroepiandrosterone (DHEA) increases territorial song and the size of an associated brain region in a male songbird.

In many species, male territorial aggression is tightly coupled with gonadal secretion of testosterone (T). In contrast, in song sparrows (Melospiza melodia morphna), males are highly aggressive during the breeding (spring) and nonbreeding (autumn and early winter) seasons, but not during molt (late summer). In aggressive nonbreeding song sparrows, plasma T levels are basal (< or = 0.10 ng/ml), and castration has no effect on aggression. However, aromatase inhibitors reduce nonbreeding aggression, indicating a role for estrogen in wintering males. In the nonbreeding season, the substrate for brain aromatase is unclear, because plasma T and androstenedione levels are basal. Aromatizable androgen may be derived from plasma dehydroepiandrosterone (DHEA), an androgen precursor. DHEA circulates at elevated levels in wintering males (approximately 0.8 ng/ml) and might be locally converted to T in the brain. Moreover, plasma DHEA is reduced during molt, as is aggression. Here, we experimentally increased DHEA in wild nonbreeding male song sparrows and examined territorial behaviors (e.g., singing) and discrete neural regions controlling the production of song. A physiological dose of DHEA for 15 days increased singing in response to simulated territorial intrusions. In addition, DHEA treatment increased the volume of a telencephalic brain region (the HVc) controlling song, indicating that DHEA can have large-scale neuroanatomical effects in adult animals. The DHEA treatment also caused a slight increase in plasma T. Exogenous DHEA may have been metabolized to sex steroids within the brain to exert these behavioral and neural effects, and it is also possible that peripheral metabolism contributed to these effects. These are the first results to suggest that exogenous DHEA increases male-male aggression and the size of an entire brain region in adults. The data are consistent with the hypothesis that DHEA regulates territorial behavior, especially in the nonbreeding season, when plasma T is basal.

Aggression↗
PubMed1996

Does functional alteration of the gonadotropic axis occur in endurance trained athletes during and after exercise? A preliminary study.

In men, the hypothalamic-pituitary-testicular axis controls the secretion of testosterone which, in this sex, is a major anabolic hormone. Physical exercise modulates testosterone concentration, affecting the whole axis by poorly understood mechanisms. We have reported in this preliminary study the short and long-term effects of exercise on the function of the gonadotropic axis in trained compared to untrained subjects. Environmental factors known to interfere with pituitary function were minimized. Four marathon and four sedentary men, were studied during 5 days successively using different combinations of two factors: duration and intensity of running tests. Day 0 (D0) was a rest day, and the exercises were: D1 and D2 brief (20 min), light (50% maximal heart rate, HRmax, D1) or intense (80% HRmax, D2), D3 and D4 prolonged (120 min) and light (50% HRmax, D3) or intense (80% HRmax, D4). Testosterone (free and total) and luteinizing hormone (LH) concentrations were measured before, during and after exercise. The baseline concentrations of plasma testosterone were lower in the long distance runners than in the sedentary group [41.8 (SEM 5.5) vs 64.5 (SEM 7.9) pmol.l-1, respectively; P < 0.05]. This phenomenon was centrally mediated as LH concentration was apparently inappropriately low [3.4 (SEM 0.4) vs 4.3 (SEM 1.0) UI.l-1; P > 0.05]. Light to moderate exercise did not modify testosterone and LH concentrations. Conversely, intense and prolonged exercise increased testosterone concentration [73.2 (SEM 9.0) vs 92 (SEM 11.0) pmol.l-1 in the long distance runners and sedentary group, respectively; P < 0.05] and lowered LH concentrations [2.1 (SEM 0.3) vs 3.4 (SEM 0.3) UI.l-1 in the long distance runners and sedentary group, respectively; P < 0.05 compared to D0, at the same time]. In our conditions of exercise, negative feedback of testosterone upon LH persisted, as positive feedback of low testosterone concentrations was apparently lacking (inappropriately low LH concentration with regard to low basal testosterone concentration).

Adult↗
PubMed1992

Ultrastructural evidence of indirect and direct autonomic innervation of human Leydig cells: comparison of neonatal, childhood and pubertal ages.

Recent physiological studies have indicated an autonomic influence on the secretion of testosterone from Leydig cells in humans and laboratory animals. Furthermore, a few studies have shown enhanced autonomic control of Leydig cell function in immature, relative to mature, laboratory animals. In the current ultrastructural study of the human testicular interstitium the morphology of autonomic components is described from neonatal, childhood and pubertal ages. Autonomic nerve fibers and varicosities with neurotransmitter vesicles are described in proximity to Leydig cells. The observed autonomic terminals are classified by vesicle morphology into three general types: (1) Type I with predominantly small agranular vesicles (30-60 nm) and occasional larger granular vesicles (100 nm). This type is morphologically consistent with being cholinergic. (2) Type II with predominantly small granular vesicles (30-60 nm), as well as sporadic large granular vesicles. These are morphologically consistent with adrenergic terminals. (3) Type III which exhibit numerous large granular vesicles of mixed size. Evidence of autonomic terminals is encountered most frequently in childhood biopsies, age 3 to 10 years. The neonatal specimen (4 months) is noteworthy in that many of the Schwann cells appear immature and no adrenergic terminals are observed. In contrast, terminals morphologically consistent with being adrenergic are common in the childhood series of biopsies. Although the vast majority of the autonomic terminals are associated with Leydig cells indirectly as "boutons en passant", separated by approximately 150 nm to more than a micron, evidence of direct contact (20 nm) of autonomic terminals with Leydig cells is presented.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Unilateral gonadal dysgenesis with both testis and fallopian tube on the same side in a 45,X/46,X inv (Y) mosaic male.

A 5-year-old male with ambiguous external genitalia, hypospadias and microphallus without an urethral orifice was referred for cytogenetic studies. Exploratory laparotomy revealed presence of an infantile uterus and unilateral gonadal dysgenesis with both testes and fallopian tube on the right side. The metaphase cells from peripheral blood culture showed both 45,X/46,X inverted Y (p11.2q11.23) cell-lines (98:2). The inverted Y was found to be of paternal origin. Maternal chromosomal pattern was normal 46,XX. The presence of a fallopian tube next to testis suggest absence of secretion of anti-Mullerian hormone by Sertoli cells. The absence of Wolffian duct derivatives suggest insufficient secretion of testosterone by Leydig cells.

Child, Preschool↗
PubMed1979

Leydig cell function in streptozotocin-induced diabetic rats.

Streptozotocin diabetic rats were infertile as a result of decreased Leydig cell function of the testes. The major changes found were: decreased number of Leydig cells and their spontaneous secretion of testosterone. No change in the receptors to LH on the Leydig cells was observed. LH was found to be obligatory for the regulation of Leydig cell function and fertility.

Animals↗
PubMed1985

FSH regulates cultured Leydig cell function via Sertoli cell proteins: an in vitro study.

The effects of follicular stimulating hormone (FSH) on testicular steroidogenic activity has been studied by testing the capacity of conditioned medium (CM) by both unstimulated (control) Sertoli cells (C-CM) and FSH stimulated Sertoli cells (FSH-CM) to influence porcine cultured Leydig cell activity. Leydig cells cultured in FSH-CM for 48 hrs, as compared to C-CM, show a significant (P less than 0.05) increase in [125I]-hCG binding (150% +/- 4) and hCG-stimulated testosterone (T) secretion (266% +/- 42). In addition, the stimulating effect of FSH-CM on Leydig cell function as compared to C-CM, is trypsin sensitive, non dialyzable, heat stable, acid resistant and is chromatographed following gel filtration (Sephadex G 100) into two different peaks of activity. These data suggest that FSH regulates Leydig cell function via (at least two types of) Sertoli cell secreted proteins.

Animals↗
PubMedDate not supplied

Cytochrome P450 changes in rats with streptozocin-induced diabetes.

It is known that the metabolism of some drugs is altered in diabetic patients and in rats with experimental diabetes induced by chemical agents, such as streptozocin. The induction and/or suppression of hepatic cytochrome P450 isozymes seen in diabetes seem to contribute to this alteration. Both metabolic and hormonal disturbances following insulin deficiency in diabetic rats are responsible for these changes. Marked changes in hepatic P450 isozymes in diabetic rats include increases in the isozymes induced by ketones and lipids, including fatty acids, and decreases in the isozymes regulated by growth hormone and testosterone. Suppressed secretion of thyroid hormones also participates in the mechanism causing these changes. Analysis of cytochrome P450 isozymes in diabetic rats is helpful in elucidating the impaired metabolism of some endogenous substrates catalyzed by the cytochrome P450, such as steroid hormones and fatty acids, in diabetes. The results of these analyses also provide insight into the prescription of drugs for diabetic patients.

Animals↗