Systemic Administration of Alcohol to Adult Rats Inhibits Leydig Cell Activity: Time Course of Effect and Role of Nitric Oxide

Herman, Melissa A.; Kang, Sang Soo; Lee, Soon; James, Peter; Rivier, Catherine

doi:10.1111/j.1530-0277.2006.00179.x

Cited by 12 publications

(7 citation statements)

References 116 publications

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“…The mechanism of ethanol suppressing testosterone levels sub-chronically is via its actions as a testicular toxin, where it can reduce testosterone synthesis rates with no negative influence on the hypothalamus signals to the testes [83,87]. Ethanol locks the functionality of Leydig cells [88] and it has been shown that necrotic Leydig cells were evident after chronic ethanol consumption [88-90]. Although, in females, the production and release of androgens occurs outside the gonads.…”

Section: Reviewmentioning

confidence: 99%

Alcohol consumption and hormonal alterations related to muscle hypertrophy: a review

Bianco

Thomas

Pomara³

et al. 2014

Nutr Metab (Lond)

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Detrimental effects of acute and chronic alcohol (ethanol) consumption on human physiology are well documented in the literature. These adversely influence neural, metabolic, cardiovascular, and thermoregulatory functions. However, the side effects of ethanol consumption on hormonal fluctuations and subsequent related skeletal muscle alterations have received less attention and as such are not entirely understood. The focus of this review is to identify the side effects of ethanol consumption on the major hormones related to muscle metabolism and clarify how the hormonal profiles are altered by such consumption.

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Section: Reviewmentioning

confidence: 99%

Alcohol consumption and hormonal alterations related to muscle hypertrophy: a review

Bianco

Thomas

Pomara³

et al. 2014

Nutr Metab (Lond)

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“…We chose the ig injection of alcohol according to a protocol previously shown to interfere with T release (Herman et al, 2006; Rivier, 1999; Selvage et al, 2004). Measurement of hypothalamic signals was used for the sake of comparison.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast to findings in the brain, both microarray and qRT-PCR methodology indicated that alcohol significantly increased Ucn 1 in the testes. As the intratesticular injection of Ucn 1 blunts the T response to hCG (Rivier, 2008), the upregulated gonadal levels of this peptide might have represented a possible mechanism mediating the inhibitory effect of this drug on Leydig cell activity (Herman et al, 2006; Rivier, 1999; Selvage et al, 2004). However, as we were unable to reverse the influence of alcohol by blocking CRF receptors (Rivier, 2008), the role played by CRF-like peptides in this model remains unresolved.…”

Section: Discussionmentioning

confidence: 99%

“…The dose chosen (4.5 g/kg, ig) induces a moderate degree of intoxication, and blood alcohol levels (BALs) in the range of those typically achieved during binge drinking (Ogilvie and Rivier, 1997), i.e., the range of BALs was 200-250 mg% 1-2 hr after ig alcohol. It also significantly inhibits T release and decreases levels of testicular steroidogenic enzymes (Herman et al, 2006; Selvage et al, 2004). …”

Section: Methodsmentioning

confidence: 99%

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Urocortins are present in the rat testis

et al. 2011

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The synthesis and release of testosterone (T) depends both on circulating luteinizing hormone (LH) and on an array of testicular factors whose role remains incompletely understood. Corticotropin-releasing factor (CRF) had been reported in the rat testes, where it was thought to inhibit T secretion. However, the discovery that the CRF-related peptides urocortins (Ucns), of which there are currently 3 subtypes (Ucn 1, 2 and 3), cross-react with many reagents previously used to detect CRF, has cast doubt on this concept. Here we show that while CRF was readily measurable in rat hypothalami (which served as controls), signals for this peptide were barely detectable in total RNA extracted from the testes. On the other hand, microarray, RT-PCR and real-time quantitative RT-PCR (qRT-PCR) analyses all indicated strong signals for Ucn 1 in the male gonads, with weaker levels of Ucn 2 and 3 mRNA gene expression. Results obtained for Ucn 1 gene expression were corroborated by immunohistochemical detection, which appeared restricted to Leydig cells. Finally, to investigate possible changes in testicular Ucn 1 levels induced by homeostatic challenges, we measured them in rats exposed to alcohol. We observed that indeed, the intragastric injection of this drug significantly increased testicular Ucn 1, but not Ucn 2, Ucn 3, CRF, CRFR1 or CRFR2 mRNA levels. Collectively, these results provide novel information regarding the presence of CRF-like peptides in the adult male rat testis.

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“…Answering these two questions was accomplished by first examining the direct effects of intra-testicular (itt) injection of NPY on the T response to human chorionic gonadotropin (hCG) administration, a model that we have extensively validated for the investigation of testicular steroidogenic function (Ogilvie and Rivier, 1998; Selvage and Rivier, 2003; Turnbull and Rivier, 1997b). We then measured testicular levels of STAR and TSPO following itt NPY administration according to protocols that we had used in other models (Herman et al, 2006; Herman and Rivier, 2006; Ogilvie et al, 1999). These two proteins were chosen because they modulate essential steps in steroidogenesis (Bauer et al, 2000; Lin et al, 1995; Papadopoulos, 1993; Payne and Hales, 2004).…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide Y acts within the rat testis to inhibit testosterone secretion

et al. 2011

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The factors that influence Leydig cell activity currently include peptides such as neuropeptide Y (NPY). In this work we investigated the ability of this compound, injected directly into the testes of adult male rats, to alter testosterone (T) release into the general circulation. At a 5 μg/kg dose administered 1 h prior to challenge with human chorionic gonadotropin (hCG, 1.0 U/kg, iv), NPY significantly (P<0.01) blunted the T response to this gonadotropin. The inhibitory effect of NPY was observed in animals pretreated with an antagonist to gonadotropin-releasing hormone or not, indicating that the decrease in plasma T found was most likely independent of pituitary luteinizing hormone. However, testicular levels of steroidogenic acute regulatory (STAR) protein or translocator protein (TSPO) in the Leydig cells did not exhibit consistent changes, which suggested that other mechanisms mediated the blunted T response to hCG. We therefore used autoradiography and immunohistochemistry methodologies to identify NPY receptors in the testes, and found them primarily located on blood vessels. Competition studies further identified these receptors as being Y 1 , a subtype previously reported to modulate the vasoconstrictor effect of NPY. The absence of significant changes in STAR and TSPO levels, as well as the absence of Y 1 receptors on Leydig cells, suggest that NPY-induced decreases in T release is unlikely to represent a direct effect of NPY on these cells. Rather, the very high expression levels of Y 1 found in testicular vessels supports the concept that NPY may alter gonadal activity, at least in part, through local vascular impairment of gonadotropin delivery to, and/or blunted T secretion from, Leydig cells.

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Systemic Administration of Alcohol to Adult Rats Inhibits Leydig Cell Activity: Time Course of Effect and Role of Nitric Oxide

Cited by 12 publications

References 116 publications

Alcohol consumption and hormonal alterations related to muscle hypertrophy: a review

Alcohol consumption and hormonal alterations related to muscle hypertrophy: a review

Urocortins are present in the rat testis

Neuropeptide Y acts within the rat testis to inhibit testosterone secretion

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