Regulation of testosterone secretion by prolactin in male rats

Huang, William J.S.; Yeh, Jiun-Yih; Tsai, Shiow-Chwen; Lin, Hong-Da; Chiao, Yu-Chung; Chen, Jiann‐Jong; Lu, Chunliang; Hwang, Seng-Wong; Wang, Shyi-Wu; Chang, Luke S.; Wang, Paulus S.

doi:10.1002/(sici)1097-4644(19990701)74:1<111::aid-jcb12>3.0.co;2-i

Cited by 22 publications

(20 citation statements)

References 31 publications

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“…In these studies with either whole testicular cells [Klemcke and Bartke, 1981] or dispersed Leydig cells [Huang et al, 1999;Sharpe and McNeilly, 1980;Waeber et al, 1983], a reduced amount of in vitro T release was noted in the hyperPRL groups in both basal and LH/hCG challenged conditions. In our previous experiments using AP-grafted hyperPRL rats, the results obtained from isolated TIC models disclosed the reduction of overall T release in the hyperPRL group [Huang et al, 1999]. These ®ndings are in agreement with the in vivo states, where reduced T release was found in the AP-grafted hyperPRL rats after the hCG stimulation.…”

Section: Discussionmentioning

confidence: 87%

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Effects of hyperprolactinemia on testosterone production in rat Leydig cells

Huang

Yeh²,

Kan³

et al. 2000

J. Cell. Biochem.

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The pathogenesis of hyperprolactinemia (hyperPRL) induced hypogonadism has been suggested to be related with a dysfunction of hypothalamus-pituitary-testis axis. While the direct inhibitory effects of prolactin (PRL) on testosterone (T) release have been demonstrated, the mechanism is still unclear. Our previous study demonstrated a diminished T release in the testicular interstitial cells (TICs) from the anterior pituitary (AP)-grafted rats as compared with the control, and the pattern was in agreement with the in vivo model. However, TICs incubation cannot totally represent the response of the Leydig cells. Therefore, a Percoll gradient purified Leydig cell model was adopted to explore the response of T release under similar challenges in this study to investigate the effects of hyperPRL on the Leydig cells per se. HyperPRL in male rats was induced by grafting rat AP under the renal capsule. The control animals were grafted with rat brain cortex tissue (CX). Six weeks after grafting, the rats were sacrificed. Either TICs or Leydig cells were isolated, respectively, for in vitro incubation and challenge. Challenge drugs included human chorionic gonadotropin (hCG, 0.05 IU/ml), steroidogenic precursors (25-OH-cholesterol, 10(-6) M; pregnenolone, 10(-6) M), forskolin (an anenylyl cyclase activator, 10(-4) M) and 8-bromo-3':5' cyclic adenosine monophosphate (cAMP) (8-Br-cAMP 10(-4) M). T released by TICs or Leydig cells was determined by radioimmunoassay. The TICs from the AP-grafted rats showed lower levels of T release than the control group while the purified Leydig cells demonstrated a reverse pattern in response to challenges of hCG, steroidogenic precursors, forskolin and 8-Br-cAMP. In hyperPRL rats, a paradoxical pattern of T release between TICs and purified Leydig cells is observed. The purified Leydig cells from AP-grafted rats demonstrated a higher level amount of T release than the control after stimulation. The phenomenon can be attributed to the change of Leydig cell sensitivity to the stimulation after the effects of chronic hyperPRL. Moreover, another possibility is the role played by other interstitial cells to modulate steroidogenesis in Leydig cells.

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Section: Discussionmentioning

confidence: 87%

“…A small slit in the renal capsule was made to allow implantation of two anterior pituitary (AP) glands in the space beneath [Everett, 1954;Huang, 1999]. Rats of the control group were implanted with a similar amount of brain cortex (CX) in a like manner.…”

Section: Induction Of Hyperprolactinemiamentioning

confidence: 99%

Effects of hyperprolactinemia on testosterone production in rat Leydig cells

Huang

Yeh²,

Kan³

et al. 2000

J. Cell. Biochem.

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“…Specific concentrations can be found in the figures or figure legends and the peptide concentrations used to approximate the dissociation constants for their receptors [26], [27], [28], [29], [30], [31], [32], [33]. DMEM complete medium consisted of Dulbecco modified Eagle medium: Nutrient mixture F12 (DMEM:F12) (Cat# 21041025, Invitrogen, Grand Island, NY) supplemented with 1× insulin, transferrin, selenium solution (Cat# I3146, Sigma-Aldrich), 1 mM sodium pyruvate (Cat# S8636, Sigma-Aldrich) and 25 mM HEPES pH7.4 (Cat# H0887, Sigma-Aldrich).…”

Section: Methodsmentioning

confidence: 99%

A Transcriptome-Wide Screen for mRNAs Enriched in Fetal Leydig Cells: CRHR1 Agonism Stimulates Rat and Mouse Fetal Testis Steroidogenesis

et al. 2012

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Fetal testis steroidogenesis plays an important role in the reproductive development of the male fetus. While regulators of certain aspects of steroidogenesis are known, the initial driver of steroidogenesis in the human and rodent fetal testis is unclear. Through comparative analysis of rodent fetal testis microarray datasets, 54 candidate fetal Leydig cell-specific genes were identified. Fetal mouse testis interstitial expression of a subset of these genes with unknown expression (Crhr1, Gramd1b, Itih5, Vgll3, and Vsnl1) was verified by whole-mount in situ hybridization. Among the candidate fetal Leydig cell-specific factors, three receptors (CRHR1, PRLR, and PROKR2) were tested for a steroidogenic function using ex vivo fetal testes treated with receptor agonists (CRH, PRL, and PROK2). While PRL and PROK2 had no effect, CRH, at low (approximately 1 to 10) nM concentration, increased expression of the steroidogenic genes Cyp11a1, Cyp17a1, Scarb1, and Star in GD15 mouse and GD17 rat testes, and in conjunction, testosterone production was increased. Exposure of GD15 fetal mouse testis to a specific CRHR1 antagonist blunted the CRH-induced steroidogenic gene expression and testosterone responses. Similar to ex vivo rodent fetal testes, ≥10 nM CRH exposure of MA-10 Leydig cells increased steroidogenic pathway mRNA and progesterone levels, showing CRH can enhance steroidogenesis by directly targeting Leydig cells. Crh mRNA expression was observed in rodent fetal hypothalamus, and CRH peptide was detected in rodent amniotic fluid. Together, these data provide a resource for discovering factors controlling fetal Leydig cell biology and suggest that CRHR1 activation by CRH stimulates rat and mouse fetal Leydig cell steroidogenesis in vivo.

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“…Antipsychotics that antagonize DA or lower DA release will thus raise serum PRL concentrations, whereas neuroactive agents that activate DA or stimulate dopaminergic receptors will lower PRL release from the pituitary. Elevated PRL can affect T production both centrally (Grattan et al 2007) and by direct actions on the Leydig cells (Huang et al 1999;Huang et al 2001). Elevated PRL may also directly affect spermatogenesis (Aleem et al 2005;Katovich et al 1985), although this effect needs to be replicated and better understood.…”

Section: Prolactinmentioning

confidence: 99%

Assessment of Circulating Hormones in Regulatory Toxicity Studies II. Male Reproductive Hormones

Chapin

Creasy²

2012

Toxicol Pathol

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When test article-related testicular toxicity or Leydig cell tumors are identified in nonclinical studies, the measurement of circulating hormones such as luteinizing hormone, follicle-stimulating hormone, inhibin, testosterone, or prolactin is often considered in order to aid mechanistic investigations or to identify potential biomarkers in man. Although some hormone levels are relatively constant, others are subject to wide variability owing to pulsatility of secretion, diurnal rhythms, and stress. To avoid being misled, it is important that this variation is factored into any study design that includes hormone measurements. Since all these possibilities start from the pathologist's reading of the tissue sections, we begin with a review of the morphologic changes that are tied to underlying alterations in hormones. We then provide the reader with basic information and representative hormone data, including coefficients of variation, for the major male reproductive hormones in the three main nonclinical species (rats, dogs, and cynomolgus monkeys). Power and probability tables for rats and dogs allow estimates of the number of animals or samples needed to provide a given likelihood of detecting a hormonal change of a given size. More importantly, we highlight the variability of this process and the real value in readers developing this information at their own site.

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Regulation of testosterone secretion by prolactin in male rats

Cited by 22 publications

References 31 publications

Effects of hyperprolactinemia on testosterone production in rat Leydig cells

Effects of hyperprolactinemia on testosterone production in rat Leydig cells

A Transcriptome-Wide Screen for mRNAs Enriched in Fetal Leydig Cells: CRHR1 Agonism Stimulates Rat and Mouse Fetal Testis Steroidogenesis

Assessment of Circulating Hormones in Regulatory Toxicity Studies II. Male Reproductive Hormones

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