Effects of prolactin on steroid production by human luteal cells in vitro

Tan, G. J. S.; Biggs, J. S. G.

doi:10.1677/joe.0.0960499

Cited by 15 publications

(6 citation statements)

References 9 publications

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“…This was also reported in the more recent study of Tan & Biggs (1983) who examined enzymatically dispersed human luteal cells.…”

Section: Discussionsupporting

confidence: 78%

“…In their study of human CL using enzymatically dispersed cells, Tan & Biggs (1983) reported that in two of the five CL examined, high prolactin levels inhibit hCG-induced oestradiol production but have no effect on progesterone. This was not found in the present study, and may be an artifact due to the method of cell dispersion.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, no effect of ovine prolactin alone could be demonstrated on progesterone production by human luteal tissue in vitro (Rice, Hammerstein & Savard, 1964;Savard, Marsh & Rice, 1965). More recently, Tan & Biggs (1983) incubated dissociated luteal cells in the presence of prolactin and again reported no effect on pro¬ gesterone production, but some inhibition of human chorionic gonadotrophin (hCG)-induced oestradiol synthesis.…”

Section: Introductionmentioning

confidence: 99%

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Prolactin stimulates steroidogenesis by human luteal tissue in vitro

Hunter¹

1984

Journal of Endocrinology

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Human luteal tissue recovered from varying stages of the luteal phase was minced and incubated for 3 h and the effect of human chorionic gonadotrophin (hCG), prolactin and hCG + prolactin on progesterone and oestradiol production measured. While hCG generally enhanced both progesterone and oestradiol synthesis, prolactin alone at either 20 or 200 micrograms/l had no significant effect on steroidogenesis. When prolactin was added along with hCG in four of six corpora lutea, however, progesterone production significantly increased and in three of six corpora lutea oestradiol production was increased above that induced by hCG alone. It is concluded that prolactin may play some role in the control of steroidogenesis by the human corpus luteum.

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“…This was also reported in the more recent study of Tan & Biggs (1983) who examined enzymatically dispersed human luteal cells.…”

Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Prolactin stimulates steroidogenesis by human luteal tissue in vitro

Hunter¹

1984

Journal of Endocrinology

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“…McNatty et al (1974) demonstrated that a high concentration of PRL in the follicular fluid may depress the progesterone secretion by granulosa cells. Higher concentrations of PRL may reduce 17b-estradiol production induced by hCG in human luteal cells in vitro (Tan & Biggs 1983). On the other hand, the production of progesterone and estrogen was higher when hCG was applied in combination with PRL than when hCG only was applied (Hunter 1984).…”

Section: Prolactin Secretion Patterns In Reproductionmentioning

confidence: 99%

Prolactin secretion patterns: basic mechanisms and clinical implications for reproduction

Egli¹,

Leeners²,

Krüger³

2010

Reproduction

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Prolactin (PRL) is one of the most versatile hormones in the mammalian body affecting reproductive, sexual, metabolic, immune, and other functions. It is therefore not surprising that the neural control of PRL secretion is complex, involving the coordinated actions of several hypothalamic nuclei. A plethora of experimental data exists on the hypothalamic control of hormone secretion under various physiological stimuli. There have been even mathematical models and computer studies published, which help to understand the complex hypothalamic-pituitary network. Nevertheless, the putative role of PRL for human reproduction still has to be clarified. Here, we review data on the underlying mechanisms controlling PRL secretion using both experimental and mathematical approaches. These investigations primarily focus on rhythmic secretion in rats during early pregnancy or pseudopregnancy, and they point to the important role of oxytocin as a crucial PRL-releasing factor. Recent data on human studies and their theoretical and clinical implications are reviewed as well. In particular, studies demonstrating a sustained PRL surge after sexual climax in males and females are presented, indicating possible implications for both sexual satiation and reproductive functions. Taking these data together, there is evidence for the hypothesis that the PRL surge induced by sexual activity, together with the altered PRL rhythmic pattern, is important for successful initialization of pregnancy not only in rodents but also possibly in humans. However, further investigations are needed to clarify such a role in humans.

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“…An important feature is luteal phase (LP) insufficiency [6,7], but it has not yet been fully established whether this is due to a direct luteolytic effect of hyperprolactinemia [8] or is a consequence of a disturbance of the hypothalamic-pituitary axis [9,10]. Prolactin (PRL) modulates steroidogenesis of human ovarian cells by exerting either a stimulatory [11,12] or an inhibitory [8,[13][14][15] effect. Some reports have indi cated a lack of a direct effect of PRL on human ovarian tissues [16,17] but the human ovary has also been shown to have specific receptors for PRL, suggesting that PRL may have a direct effect on ovarian function [18][19][20].…”

Section: Introductionmentioning

confidence: 99%

Effect of Luteal Metoclopramide-Induced Hyperprolactinemia on Pituitary and Luteal Responsiveness to Gonadotropin-Releasing Hormone

Caruso

Lanzone²,

Fulghesu³

et al. 1989

Horm Res

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The pituitary and corpus luteum responses to acute gonadotropin-releasing hormone (GnRH) administration at the mid-luteal phase (LP) were studied in 24 infertile women. Patients were randomly divided into two groups. In one group (n = 12) metoclopramide (MCP, 10 mg orally 3 times daily) was administered from day 0 or 1 of the LP for 7 days. On day 7 or 8 of LP blood samples were taken every 15 min for 180 min; then 25 µg GnRH were acutely administered intravenously and blood samples taken at 185, 195, 210, 225, 240, 255, 270, 285 and 300 min. In the other 12 patients the same experimental design was performed on day 7 or 8 of an untreated LP. Plasma prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), progesterone and estradiol (E₂) were assayed. The responsiveness of the different hormones to GnRH was evaluated as the integrated secretory area for 120 min after injection (sISA = stimulated integrated secretory area) and as the percentage increase (ΔA) with respect to the area under basal conditions before GnRH administration (bISA = basal integrated secretory area). MCP-treated women showed higher basal PRL levels (p < 0.01) and lower basal plasma concentrations and bISA (p < 0.01) values of LH than controls. After GnRH a more marked response of LH secretion was observed in the treated group (p < 0.01), so that the absolute values of sISA were superimposable in both groups. Basal and stimulated FSH secretion did not differ significantly in the study groups. Basal plasma and bISA values of progesterone were also decreased in MCP-treated subjects. After GnRH injection the absolute values of progesterone sISA were greater in controls (p < 0.01), but ΔA values were similar in both groups. Basal and stimulated E₂ secretion was also superimposable in both groups. In conclusion, mild MCP-induced hyperprolactinemia during LP affects the hypothalamic-pituitary axis by a derangement of gonadotropin secretion which in turn determines a blunted functional activity of the corpus luteum.

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Effects of prolactin on steroid production by human luteal cells in vitro

Cited by 15 publications

References 9 publications

Prolactin stimulates steroidogenesis by human luteal tissue in vitro

Prolactin stimulates steroidogenesis by human luteal tissue in vitro

Prolactin secretion patterns: basic mechanisms and clinical implications for reproduction

Effect of Luteal Metoclopramide-Induced Hyperprolactinemia on Pituitary and Luteal Responsiveness to Gonadotropin-Releasing Hormone

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