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Testosterone Production (testosterone + production)

Distribution by Scientific Domains

Medical Sciences	84%

Selected Abstracts

Human sebocytes express prostaglandin E2 receptors EP2 and EP4 but treatment with prostaglandin E2 does not affect testosterone production

BRITISH JOURNAL OF DERMATOLOGY, Issue 3 2009
W. Chen
Summary Background, Prostaglandins (PG) play an important role in cutaneous homeostasis. Among other skin cells, human sebocytes express cyclooxygenases and can produce PGE2. Various prostanoid receptors have been demonstrated in epidermis and hair follicles, while limited data are available regarding their expression in sebaceous glands. In addition, the interaction between PGE2 and androgenesis remains largely unclear. Objectives, To examine the expression of PGE2 receptor (EP) and PGF2, receptor (FP) in human sebocytes and the influence of PGE2 or PGF2, on testosterone production. Methods, A reverse transcription-polymerase chain reaction study was used to detect the expression of EP subtypes and FP. A testosterone radioimmunoassay was used to measure the amount of testosterone in the supernatant of cultured SZ95 sebocytes treated with PGE2 or PGF2, alone or in the presence of various androgen precursor substrates. Results, SZ95 sebocytes expressed mainly EP2 and EP4 but not EP3 or FP. Testosterone production was not induced by PGE2 or PGF2,, alone or in the presence of cholesterol. PGE2 did not affect androgenesis in cultured sebocytes. Conclusions, The expression patterns of prostanoid receptors differ between sebocytes, hair follicles and epidermis. The effects of PGE2 and PGF2, on the proliferation, lipogenesis and inflammation of sebocytes appear not to be associated with androgenesis. [source]

Chronic hypothyroidism only marginally affects adult-type Leydig cell regeneration after EDS administration

INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 1 2010
Eddy Rijntjes
Summary Chronic prenatally induced dietary hypothyroidism delays adult-type Leydig cell development, but does not block this process. Using a chemical model to induce hypothyroidism, it was suggested that development of a new population of Leydig cells was completely inhibited following the addition of the cytotoxic compound ethane-1,2-dimethyl sulphonate (EDS). In this study, we used a dietary approach to induce hypothyroidism and reinvestigated the regeneration of the Leydig cell population following EDS administration. Eighty-four day old euthyroid and chronically hypothyroid rats received an injection of EDS and were killed directly before or at regular intervals up to 77 days after EDS. In some control and hypothyroid animals, the first progenitor-type Leydig cells were observed at day 12 after EDS. At day 16, Leydig cell progenitors were present in all rats. The percentage of proliferating Leydig cells peaked in the euthyroid animals at day 21 after EDS. In the hypothyroid testis such a peak was not observed, although the percentage of proliferating regenerating Leydig cells was significantly higher from days 35 to 56 compared with the controls. This suggested that the wave of Leydig cell proliferation was delayed in the hypothyroid animals as compared with the euthyroid controls. On the day of EDS injection, the Leydig/Sertoli cell ratio was 37% lower in the hypothyroid rats compared with the controls. The Leydig/Sertoli cell ratio remained lower in the EDS-treated hypothyroid animals compared with the controls at all time points investigated. At day 77 after EDS, the Leydig cell population had returned to its pre-treatment size in both groups. Plasma testosterone production was reduced to below detectable levels immediately after EDS injection, and started to increase again on day 16, reaching pre-treatment values on day 21 in both groups. Taken together, severely reduced thyroid hormone levels did not block the regeneration of the adult-type Leydig cell population following EDS, as has been suggested previously. [source]

Lipoprotein lipase and endothelial lipase in human testis and in germ cell neoplasms

INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 1 2010
J. E. Nielsen
Summary The aim of this study was to investigate endothelial lipase (EL, LIPG) and lipoprotein lipase (LPL) mRNA and protein expression in normal human testis and testicular germ cell tumours (GCT). Both EL and LPL were expressed in normal seminiferous tubules and in the interstitial compartment. EL mRNA and protein were found in all germ cells as well as in Sertoli and Leydig cells. EL mRNA was abundant in pre-invasive carcinoma in situ (CIS) cells and GCTs, and EL protein was present in the cytoplasm of these cells. LPL mRNA was also relatively abundant in germ cells, Sertoli cells, CIS cells and GCTs. The LPL protein, however, was restricted to the cell membranes of pachytene spermatocytes and spermatids in normal tubules, absent from CIS cells and scarcely represented in tumours. The distribution of LPL protein in non-seminomas resembled the distribution of OCT3/4, a marker of embryonal carcinoma. The results suggest that both EL and LPL participate in the supply of nutrients and steroidogenesis in the testes, and that especially EL may be important for the supply of cholesterol for testosterone production in the Leydig cells. The partial cellular separation of the expression of the two lipases in normal testis suggests the existence of distinct biological roles, perhaps developmentally regulated, as indicated by the LPL expression in GCTs with embryonic features. A high expression of EL and abundance of lipid in tubules with CIS may have a diagnostic value. [source]

Suppression of testosterone stimulates recovery of spermatogenesis after cancer treatment

INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 3 2003
Marvin L. Meistrich
Summary It is important to develop methods to prevent or reverse the infertility caused by chemotherapy or radiation therapy for cancer in men. Radiation and some chemotherapeutic agents kill spermatogonial stem cells, but we have shown that these cells survive in rats, although they are unable to differentiate. There is evidence that this phenomenon also occurs in men. The block to spermatogonial differentiation in rats is caused by some unknown change, either in the spermatogonia or the somatic elements of the testis, such that testosterone inhibits spermatogonial differentiation. In the rat, the spermatogenesis and fertility lost following treatment with radiation or some chemotherapeutic agents can be restored by suppressing testosterone with gonadotropin releasing hormone (GnRH) agonists or antagonists, either before or after the cytotoxic insult. The applicability of this procedure to humans is still unknown. Some anticancer regimens may kill all the stem cells, in which case the only option would be spermatogonial transplantation. However, in some cases stem cells survive and there is one report of stimulation of recovery of spermatogenesis with hormonal treatment. Clinical trials should focus on treating patients with hormones during or soon after anticancer treatment. The hormone regimen should involve suppression of testosterone production with minimum androgen supplementation used to improve the diminished libido. [source]

The ,oestrogen hypothesis', where do we stand now?,

INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 1 2003
Richard M. Sharpe
Summary The original ,oestrogen hypothesis' postulated that the apparent increase in human male reproductive developmental disorders (testis cancer, cryptorchidism, hypospadias, low sperm counts) might have occurred because of increased oestrogen exposure of the human foetus/neonate; five potential routes of exposure were considered. This review revisits this hypothesis in the light of the data to have emerged since 1993. It addresses whether there is a secular increasing trend in the listed disorders and highlights the limitations of available data and how these are being addressed. It considers whether new data has emerged to support the suggestion that increased oestrogen exposure could cause these abnormalities and reviews new data on potential routes via which such increased exposure could have occurred. Secular trends: The disorders listed above are now considered to represent a syndrome of disorders (testicular dysgenesis syndrome, TDS) with a common origin in foetal life. Testicular cancer has increased in incidence in Caucasian men worldwide and lifetime risk is 0.3,0.8%. Secular trends in cryptorchidism are unclear but it is by far the commonest (2,4% at birth) congenital abnormality in either sex. Secular trends for hypospadias are not robust, although most studies suggest a progressive increase; registry data probably under-estimates incidence, but based on this data hypospadias is the second most common (0.3,0.7% at birth) congenital malformation. Retrospective analyses of sperm count data show a global downward trend but this is inconclusive , prospective studies using standardized methodology show significant differences between countries and very low sperm counts in the youngest cohort of men. For all disorders, other then testis cancer, standardized prospective studies are the best way forward and are in progress across Europe. Oestrogen effects: Evidence that foetal exposure to oestrogens can induce the above disorders has strengthened. New pathways via which such changes could be induced have been identified, including suppression of testosterone production by the foetal testis, suppression of androgen receptor expression and suppression of insulin-like factor-3 (InsL3) production by foetal Leydig cells. Other evidence suggests that the balance between androgen and oestrogen action may be important in induction of reproductive tract abnormalities. Oestrogen exposure: Although many new environmental oestrogens have been identified, their uniformly weak oestrogenicity excludes the possibility that they could induce the above disorders. However, emerging data implicates various environmental chemicals in being able to alter endogenous levels of androgens (certain phthalates) and oestrogens (polychlorinated biphenyls, polyhalogenated hydrocarbons), and the former have been shown to induce a similar collection of disorders to TDS. Other mechanisms via which increased fetal exposure to pregnancy oestrogens might occur (increasing trend in obesity, dietary changes) are also discussed. [source]

Specificity of a new lipid mediator produced by testicular and peritoneal macrophages on steroidogenesis

INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 5 2000
Lukyanenko
Macrophage-derived factor (MDF) is a lipophilic factor produced by rat testicular and peritoneal macrophages that maximally stimulates testosterone production by rat Leydig cells through a steroidogenic acute regulatory protein independent mechanism. The purpose of the present study was to determine whether MDF is also produced by human macrophages, and/or if it acts on human steroidogenic cells. We also studied the tissue-specific functions of MDF by determining if it also acts on steroidogenic cells of the ovary and adrenal glands and, if so, does it require new protein synthesis. It was found that MDF was produced by human peritoneal macrophages, and was capable of stimulating human steroidogenic cells. In terms of tissue specificity, it was found that primary cultures of rat adrenocortical cells respond to MDF with increased secretion of aldosterone and corticosterone, as did rat granulosa cells by producing progesterone. MDF acted in the presence of cycloheximide, indicating that it does not require new protein synthesis. These results indicate that MDF may have significant therapeutic potential and provide a basis for future studies concerning its physiological role in humans. These results further suggest that MDF is not only involved in paracrine regulation of Leydig cells, but also has the potential for the local regulation of steroidogenesis in both granulosa and adrenal cortical cells. [source]

Assessment of urinary total testosterone production by a highly sensitive time-resolved fluorescence immunoassay ,

JOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 6 2008
Shihua Bao
Abstract Radioimmunoassay (RIA) that involves purification of the analyte by organic solvent extraction is widely used. Although the extraction RIA is reliable when properly validated, it is time consuming and radioactive, we measure urinary total testosterone with a highly sensitive rapid and accurate time-resolved fluorescence immunoassay (TRFIA) method. High affinity antitestosterone antibody and Eu3+ labeled Donkey antisheep IgG as tracers were used. The assay was evaluated for specificity, sensitivity, analytical recovery, precision and dilution linearity by the TRFIA method on urine samples. A satisfactory standard curve for testosterone TRFIA has been developed with good sensitivity (5.1,pmol/L). The validity of the assay for urinarytotal testosterone was confirmed by thegood correlation between the results obtained by TRFIA (X) and those RIA (Y) (Y=0.075+0.971X, R=0.992). Specificity, analytical recovery, precision and dilution linearity studies were determined and all found to be satisfactory. Male urinary total testosterone excretion ranged from 64.00 to 374.11,nmol/24,hr, which was about four times more than the range for women urinary testosterone excretion (14.16,100.65,nmol/24,hr), which suggests that a direct, reliable, easy to automate, highly sensitive and specific TRFIA type assay for the measurement of total testosterone in urine samples has been developed. J. Clin. Lab. Anal. 22:403,408, 2008. © 2008 Wiley-Liss, Inc. [source]

Ontogeny of the androgen receptor expression in the fetal and postnatal testis: Its relevance on Sertoli cell maturation and the onset of adult spermatogenesis

MICROSCOPY RESEARCH AND TECHNIQUE, Issue 11 2009
Rodolfo A. Rey
Abstract From fetal life to adulthood, the testis evolves through maturational phases showing specific morphologic and functional features in its different compartments. The seminiferous cords contain Sertoli and germ cells, surrounded by peritubular cells, and the interstitial tissue contains Leydig cells and connective tissue. Sertoli cells secrete anti-Müllerian hormone (AMH), whereas Leydig cells secrete androgens. In the fetal and early postnatal testis, Leydig cells actively secrete androgens. Sertoli cells are morphologically and functionally immature,e.g., they secrete high levels of AMH,and germ cells proliferate by mitosis but do not enter meiosis. During infancy and childhood, Leydig cells regress and testosterone secretion declines dramatically. Sertoli cells remain immature and spermatogenesis is arrested at the premeiotic stage. At puberty, Leydig cells differentiate again, and testosterone concentration increases and provokes Sertoli cell maturation,e.g., down-regulation of AMH expression,and germ cells undergo meiosis, the hallmark of adult spermatogenesis driving to sperm production. An intriguing feature of testicular development is that, although testosterone production is as active in the fetal and early postnatal periods as in puberty, Sertoli cells and spermatogenesis remain immature until pubertal onset. Here, we review the ontogeny of the androgen receptor expression in the testis and its impact on Sertoli cell maturation and the onset of pubertal spermatogenesis. We show that the absence of androgen receptor expression in Sertoli cells underlies a physiological stage of androgen insensitivity within the male gonad in the fetal and early postnatal periods. Microsc. Res. Tech., 2009. © 2009 Wiley-Liss, Inc. [source]

Role of gonadotropin-releasing hormone (GnRH) in the regulation of gonadal differentiation in the gilthead seabream (Sparus aurata)

MOLECULAR REPRODUCTION & DEVELOPMENT, Issue 1 2007
L. Soverchia
Abstract It has been proposed that gonadotropin-releasing hormone (GnRH) plays an autocrine/paracrine regulatory role in mammalian and fish ovaries. The marine teleost gilthead seabream is an interesting model since, during the life span of the fish, gonadal tissues develop first as testes, which then regress allowing the development of ovarian follicles. Recent studies carried out in ovaries of the gilthead seabream have demonstrated that various GnRH transcripts as well as GnRH splicing variants are expressed. The mRNA level of several GnRH forms in the female and male areas of the switching gonad, and their possible role in this process, were further investigated. The results here reported show that sGnRH, cGnRH-II, and sbGnRH transcripts are locally expressed during gilthead seabream gonadal differentiation; the expression of the three GnRH forms was found to differ among the morphologically defined areas of the switching gonad, as demonstrated by applying reverse transcription-polymerase chain reaction (RT-PCR), together with in situ hybridization, and semiquantitative PCR analyses. Moreover, the hypothesis that GnRH forms may regulate testicular regression via an apoptotic mechanism was investigated by analyzing the different areas of switching gonads for caspase-3 activity as a measure of apoptosis. Our results showed a marked increase of caspase-3 activity in the area corresponding to the regressing testes in which a significant decrease of testosterone production was also found. The present findings demonstrate that the changes in the endogenous GnRH transcripts could be related with the gonadal differentiation in gilthead seabream, and that exogenous GnRH plays a role by stimulating apoptosis in the degenerating testis. Mol. Reprod. Dev. 74: 57,67, 2007. © 2006 Wiley-Liss, Inc. [source]

Hormonal Changes in Menopause and Implications on Sexual Health

THE JOURNAL OF SEXUAL MEDICINE, Issue 2007
Anneliese Schwenkhagen MD
ABSTRACT Introduction., The menopause is characterized by an array of changes to the female body caused by modulations which occur in the production of estrogens and androgens. The ovaries are important sites of testosterone production in the peri- and postmenopausal women, but the contribution of testosterone pro-hormones from the adrenal glands falls precipitously to the extent where the ovaries cannot correct the deficit. This results in a net decline in circulating testosterone levels. Aims., This paper gives an overview of this interesting subject area. Researchers have cogitated on the relationship between the physical effects of the menopause and the observed declines in testosterone levels, but it is now much clearer that falling testosterone levels cannot explain all of these changes. Main Outcome Measures., The cessation of follicular functioning results in a steep decline in the production of estrogens. This modulation is responsible for the physical manifestations of the menopause,hot flushes, sleep disturbances, mood changes, bleeding problems, local urogenital problems, vaginal changes, etc. Methods., A review of the pertinent literature was conducted to investigate hormonal changes around the menopause. A précis of the salient information is presented here. Results., Although the most obvious and well-known effects of the menopause are due to the decline of estrogen levels, the effects of falling testosterone levels are subtle, but by no means less significant. Reductions in sexual motivation, sexual arousal, vaginal lubrication, etc. are all associated with plummeting androgen levels. Conclusions., Today, several options exist for the treatment of the endocrinological changes associated with the menopause. Estrogen deficiency can be corrected with hormone replacement therapy and topical preparations for the genitalia. A new transdermal system for the administration of testosterone shows a great deal of potential for the treatment of androgen deficiency. Schwenkhagen A. Hormonal changes in menopause and implications on sexual health. J Sex Med 2007;4(suppl 3):220,226. [source]

Sensitivity Analysis for Nonrandom Dropout: A Local Influence Approach

BIOMETRICS, Issue 1 2001
Geert Verbeke
Summary. Diggle and Kenward (1994, Applied Statistics43, 49,93) proposed a selection model for continuous longitudinal data subject to nonrandom dropout. It has provoked a large debate about the role for such models. The original enthusiasm was followed by skepticism about the strong but untestable assumptions on which this type of model invariably rests. Since then, the view has emerged that these models should ideally be made part of a sensitivity analysis. This paper presents a formal and flexible approach to such a sensitivity assessment based on local influence (Cook, 1986, Journal of the Royal Statistical Society, Series B48, 133,169). The influence of perturbing a missing-at-random dropout model in the direction of nonrandom dropout is explored. The method is applied to data from a randomized experiment on the inhibition of testosterone production in rats. [source]