Differentiation of Adult Leydig Cells in the Neonatal Rat Testis Is Arrested by Hypothyroidism1

Mendis‐Handagama, S. M. L. C.; Ariyaratne, H.; Manen, K. R. Teunissen Van; Haupt, R

doi:10.1095/biolreprod59.2.351

Cited by 75 publications

(101 citation statements)

References 29 publications

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“…It was previously reported that FLCs decline in number after birth, a cellular process suggested to be associated with: (a) cell death (Kuopio et al, 1989), (b) dedifferentiation to fibroblastictype cells (Gondos et al, 1974) or (c) transformation to adult-type Leydig cell population (Mendis-Handagama et al, 1998). However, several studies suggested that PFLCs do not all enter apoptosis and degenerate but can persist in later puberty (Kerr and Knell, 1988;Ariyaratne and Chamindrani Mendis-Handagama, 2000;Ivell et al, 2003).…”

Section: Effect Of (Bu) 2 Camp and Paracrine Factors On Pflc Prolifermentioning

confidence: 99%

Steroidogenesis and steroidogenic gene expression in postnatal fetal rat Leydig cells

Weisser¹,

Landreh²,

Söder³

et al. 2011

Molecular and Cellular Endocrinology

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Please cite this article as: Weisser, J., Landreh, L., Söder, O., Svechnikov, K., Steroidogenesis and steroidogenic gene expression in postnatal fetal rat Leydig cells, Molecular and Cellular Endocrinology (2008), doi:10.1016/j.mce.2011 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Our data indicate that cAMP-activated signaling pathway(s) play an important role in the regulation of PFLCs differentiation and function.

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Section: Effect Of (Bu) 2 Camp and Paracrine Factors On Pflc Prolifermentioning

confidence: 99%

Steroidogenesis and steroidogenic gene expression in postnatal fetal rat Leydig cells

Weisser¹,

Landreh²,

Söder³

et al. 2011

Molecular and Cellular Endocrinology

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“…differentiation into adult Leydig cells in neonatal prepubertal rats [4,5]. In addition, daily injections of T3 to neonatal prepubertal rats accelerates the differentiation of Leydig cells [5].…”

mentioning

confidence: 97%

Effect of Methimazole-induced Hypothyroidism on Adrenal and Gonadal Functions in Male Japanese Quail (<i>Coturnix japonica</i>)

Wang

Saita

Watanabe

et al. 2007

Journal of Reproduction and Development

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Abstract.To investigate the effect of hypothyroidism on gonadal and adrenal functions in male Japanese quail (Coturnix japonica), hypothyroidism was induced in male adult Japanese quail by daily administration of 2-Mercapto-1-methylimidazole (methimazole) in their drinking water. Four weeks after methimazole treatment, the Japanese quail were scarificed, and the plasma concentrations of free triiodothyronine (FT3), free thyroxine (FT4), total T3 (TT3), total T4 (TT4), corticosterone, testosterone, LH and immunoreactive (ir) inhibins were measured by radioimmunoassy, the testes and adrenal glands were removed and weighed and the thyroid glands and testes were fixed in 4% paraformaldehyde for histological observation. The results showed that the hypothyroidism induced by methimazole caused a significant decrease in body and testes weight; the plasma levels of FT3, FT4 and TT4 significantly decreased, and the hypothyroid quail possessed a greater number of small follicles and more follicular epithelial cells in the thyroid gland. In addition, hypothyroidism resulted in a significant decrease in the plasma concentrations of corticosterone, LH, testosterone and irinhibin. Furthermore, no spermatogenesis was found in the seminiferous tubules of the methimazole treatment groups. These results clearly demonstrate that hypothyroidism caused both gonadal and adrenal disturbances in the adult male Japanese quail.

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“…These changes were caused by a prolongation of Sertoli cell proliferation and a delay in Sertoli cell differentiation (9,18,42,52). At the same time, under these hypothyroid conditions, progenitor-type Leydig cell formation was reported to be arrested up to 21 days after birth in rats (27). Following cessation of the hypothyroid condition at the age of 26 days, developing adult-type Leydig cells started to proliferate massively (Teerds KJ, unpublished data), leading to an approximate 70% increase in the Leydig cell population in adulthood (14,46).…”

mentioning

confidence: 98%

Prenatal induced chronic dietary hypothyroidism delays but does not block adult-type Leydig cell development

Rijntjes

Swarts²,

Anand‐Ivell³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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Rijntjes E, Swarts HJ, Anand-Ivell R, Teerds KJ. Prenatal induced chronic dietary hypothyroidism delays but does not block adult-type Leydig cell development. Am J Physiol Endocrinol Metab 296: E305-E314, 2009. First published November 25, 2008 doi:10.1152/ajpendo.90750.2008.-Transient hypothyroidism induced by propyl-2-thiouracyl blocks postpartum Leydig cell development. In the present study, the effects of chronic hypothyroidism on the formation of this adult-type Leydig cell population were investigated, using a more physiological approach. Before mating, dams were put on a diet consisting of an iodide-poor feed supplemented with a low dose of perchlorate and, with their offspring, were kept on this diet until death. In the pups at day 12 postpartum, plasma thyroid-stimulating hormone levels were increased by 20-fold, whereas thyroxine and free tri-iodothyronine levels were severely depressed, confirming a hypothyroid condition. Adult-type progenitor Leydig cell formation and proliferation were reduced by 40 -60% on days 16 and 28 postpartum. This was followed by increased Leydig cell proliferation at later ages, suggesting a possible slower developmental onset of the adult-type Leydig cell population under hypothyroid conditions. Testosterone levels were increased 2-to 10-fold in the hypothyroid animals between days 21 and 42 postpartum compared with the age-matched controls. Combined with the decreased presence of 5␣-reductase, this implicates a lower production capacity of 5␣-reduced androgens. In 84-day-old rats, after correction for body weight-to-testis weight ratio, plasma insulin-like factor-3 levels were 35% lower in the hypothyroid animals, suggestive of a reduced Leydig cell population. This is confirmed by a 37% reduction in the Sertoli cell-to-Leydig cell ratio in hypothyroid rats. In conclusion, we show that dietary-induced hypothyroidism delays but, unlike propyl-2-thiouracyl, does not block the development of the adult-type Leydig cell population.

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Differentiation of Adult Leydig Cells in the Neonatal Rat Testis Is Arrested by Hypothyroidism1

Cited by 75 publications

References 29 publications

Steroidogenesis and steroidogenic gene expression in postnatal fetal rat Leydig cells

Steroidogenesis and steroidogenic gene expression in postnatal fetal rat Leydig cells

Effect of Methimazole-induced Hypothyroidism on Adrenal and Gonadal Functions in Male Japanese Quail (<i>Coturnix japonica</i>)

Prenatal induced chronic dietary hypothyroidism delays but does not block adult-type Leydig cell development

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