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Titolo:
Effects of hyperprolactinemia on testosterone production in rat Leydig cells
Autore:
Huang, WJ; Yeh, JY; Kan, SF; Chang, LS; Wang, PS;
Indirizzi:
Natl Yang Ming Univ, Sch Life Sci, Dept Physiol, Taipei 11221, Taiwan NatlYang Ming Univ Taipei Taiwan 11221 pt Physiol, Taipei 11221, Taiwan Natl Yang Ming Univ, Sch Med, Inst Clin Res, Taipei 11221, Taiwan Natl Yang Ming Univ Taipei Taiwan 11221 t Clin Res, Taipei 11221, Taiwan Vet Gen Hosp, Dept Surg, Div Urol, Taipei 11217, Taiwan Vet Gen Hosp Taipei Taiwan 11217 pt Surg, Div Urol, Taipei 11217, Taiwan
Titolo Testata:
JOURNAL OF CELLULAR BIOCHEMISTRY
fascicolo: 3, volume: 80, anno: 2001,
pagine: 313 - 320
SICI:
0730-2312(2001)80:3<313:EOHOTP>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
CYCLIC-AMP PRODUCTION; LUTEINIZING-HORMONE; TESTICULAR MACROPHAGES; INTERSTITIAL-TISSUE; BINDING-SITES; LH-RECEPTOR; PROLACTIN; TESTIS; SECRETION; INVITRO;
Keywords:
prolactin; hyperprolactinemia; leydig cells; testosterone; testicular interstitial cells; male rats;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Wang, PS Natl Yang Ming Univ, Sch Life Sci, Dept Physiol, Shih Pai, Taipei11221, Taiwan Natl Yang Ming Univ Shih Pai Taipei Taiwan 11221 i 11221, Taiwan
Citazione:
W.J. Huang et al., "Effects of hyperprolactinemia on testosterone production in rat Leydig cells", J CELL BIOC, 80(3), 2001, pp. 313-320

Abstract

The pathogenesis of hyperprolactinemia (hyperPRL) induced hypogonadism hasbeen 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 perse. 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 TICsor 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 sensitivityto 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. (C) 2001 Wiley-Liss, inc.

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Documento generato il 06/04/20 alle ore 08:13:42