Long-term feeding of hydroalcoholic extract powder ofLepidium meyenii(maca) enhances the steroidogenic ability of Leydig cells to alleviate its decline with ageing in male rats

ABSTRACT The long-term effects of oxytocin administration on the testis were studied using intratesticular implants. Adult male rats had an Accurel device containing 20 μg oxytocin (releasing approximately 200 ng/day) implanted into the parenchyma of each testis; control animals received empty devices. The animals were killed at weekly intervals for 4 weeks. Some animals were perfused and the testes processed for light and electron microscopy. Blood was collected from the remaining animals for the measurement of testosterone, dihydrotestosterone, LH, FSH and oxytocin; epididymal sperm counts were measured and the testes were extracted and radioimmunoassayed for testosterone, dihydrotestosterone and oxytocin. Long-term administration of oxytocin resulted in a significant reduction in testicular and plasma testosterone levels throughout the 4-week period examined and, after 14 days of treatment, lipid droplets were seen in the Leydig cells of treated but not control animals. Concentrations of dihydrotestosterone in the plasma and testes of the oxytocin-treated animals, however, were significantly elevated after 7 and 14 days and at no time fell below control values. Plasma FSH levels were also lower in the oxytocin-treated animals. Intratesticular oxytocin treatment did not affect LH or oxytocin concentrations in the plasma, epididymal sperm counts or the number of Leydig cells in the testis. Empty Accurel devices had no effect on testicular morphology. This study provides the first evidence that oxytocin in vivo can modify steroidogenesis in the testis. Journal of Endocrinology (1991) 130, 231–238

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Feeding hydroalcoholic extract powder ofLepidium meyenii(maca) increases serum testosterone concentration and enhances steroidogenic ability of Leydig cells in male rats

Andrologia ◽

10.1111/and.12453 ◽

2015 ◽

Vol 48 (3) ◽

pp. 347-354 ◽

Cited By ~ 12

Author(s):

Y. Ohta ◽

K. Yoshida ◽

S. Kamiya ◽

N. Kawate ◽

M. Takahashi ◽

...

Keyword(s):

Leydig Cells ◽

Serum Testosterone ◽

Male Rats ◽

Hydroalcoholic Extract ◽

Testosterone Concentration

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Differential effects of the administration of human chorionic gonadotropin to postnatal rats

Journal of Endocrinology ◽

10.1677/joe.0.1420527 ◽

1994 ◽

Vol 142 (3) ◽

pp. 527-534 ◽

Cited By ~ 12

Author(s):

F Gaytan ◽

L Pinilla ◽

J L Romero ◽

E Aguilar

Keyword(s):

Chorionic Gonadotropin ◽

Human Chorionic Gonadotropin ◽

Leydig Cells ◽

Reproductive Function ◽

Male Rats ◽

Testicular Development ◽

Long Term Effects ◽

Adult Type ◽

Short And Long Term

Abstract Neonatal and prepubertal male rats were treated with human chorionic gonadotropin (hCG, 5 IU/g body weight per day) on days 2–4 or 20–22. Depending on the date of treatment, different groups of rats were sacrificed at 5, 23, 30 and 100 days of age, in order to study the short-and long-term effects of the treatment with hCG on the development of the testes and sex accessory organs. Rats treated with hCG on days 2–4 showed increased number and size of foetal Leydig cells at 5 days of age. However, long-term effects include decreased numbers of adult-type Leydig cells, decreased weight of the testes and sex accessory organs, decreased basal and hCG-stimulated testosterone secretion, and delayed balano-preputial separation. In contrast, animals treated with hCG on days 20–22 showed similar short- and long-term effects, consisting of increased number of adult-type Leydig cells and macrophages, increased weight of the testes and sex accessory organs and advanced balano-preputial separation. In adulthood, both groups showed normal reproductive function. These results seem to indicate that the effects of hCG treatment in prepubertal rats are dependent on the type of Leydig cell stimulated, and suggest that foetal Leydig cells play a regulatory role in the early postnatal testicular development. Journal of Endocrinology (1994) 142, 527–534

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Faculty Opinions recommendation of Long term facilitation of respiratory motor output decreases with age in male rats.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718021187.793478915 ◽

2013 ◽

Author(s):

Frank L Powell

Keyword(s):

Motor Output ◽

Male Rats ◽

Long Term Facilitation

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Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy

Biological Research ◽

10.1186/s40659-021-00328-4 ◽

2021 ◽

Vol 54 (1) ◽

Author(s):

Mayarling Francisca Troncoso ◽

Mario Pavez ◽

Carlos Wilson ◽

Daniel Lagos ◽

Javier Duran ◽

...

Keyword(s):

Glucose Metabolism ◽

Cardiac Hypertrophy ◽

Glucose Uptake ◽

Male Rats ◽

Cardiomyocyte Hypertrophy ◽

Mrna Levels ◽

Elevated Glucose ◽

Amp Activated Protein Kinase ◽

Cultured Cardiomyocytes

Abstract Background Testosterone regulates nutrient and energy balance to maintain protein synthesis and metabolism in cardiomyocytes, but supraphysiological concentrations induce cardiac hypertrophy. Previously, we determined that testosterone increased glucose uptake—via AMP-activated protein kinase (AMPK)—after acute treatment in cardiomyocytes. However, whether elevated glucose uptake is involved in long-term changes of glucose metabolism or is required during cardiomyocyte growth remained unknown. In this study, we hypothesized that glucose uptake and glycolysis increase in testosterone-treated cardiomyocytes through AMPK and androgen receptor (AR). Methods Cultured cardiomyocytes were stimulated with 100 nM testosterone for 24 h, and hypertrophy was verified by increased cell size and mRNA levels of β-myosin heavy chain (β-mhc). Glucose uptake was assessed by 2-NBDG. Glycolysis and glycolytic capacity were determined by measuring extracellular acidification rate (ECAR). Results Testosterone induced cardiomyocyte hypertrophy that was accompanied by increased glucose uptake, glycolysis enhancement and upregulated mRNA expression of hexokinase 2. In addition, testosterone increased AMPK phosphorylation (Thr172), while inhibition of both AMPK and AR blocked glycolysis and cardiomyocyte hypertrophy induced by testosterone. Moreover, testosterone supplementation in adult male rats by 5 weeks induced cardiac hypertrophy and upregulated β-mhc, Hk2 and Pfk2 mRNA levels. Conclusion These results indicate that testosterone stimulates glucose metabolism by activation of AMPK and AR signaling which are critical to induce cardiomyocyte hypertrophy.

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