Inhibition of Recovery of Spermatogenesis in Irradiated Rats by Different Androgens

Shetty, Gunapala; Wilson, Gene; Hardy, Matthew P.; Niu, En‐Mei; Huhtaniemi, Ilpo; Meistrich, Marvin L.

doi:10.1210/en.2002-220206

Cited by 52 publications

(43 citation statements)

References 47 publications

(38 reference statements)

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“…Because endogenous testosterone levels are relatively constant, mimicking them is simple. Endogenous testosterone levels in adult rats vary according to age, strain, etc., from ϳ1-7 ng/ml, and near-physiological replacement is usually achieved with constant-release silicone-capsule implants (117,118,659). Because reproductive hormone levels cycle in female rats, however, constant-release pellets cannot be considered physiological.…”

Section: Physiological Sex Differences In Disordered Eating)mentioning

confidence: 99%

Sex differences in the physiology of eating

Asarian

Geary²

2013

American Journal of Physiology-Regulatory, Integrative and Comp

408

349

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(HPG) axis function fundamentally affects the physiology of eating. We review sex differences in the physiological and pathophysiological controls of amounts eaten in rats, mice, monkeys, and humans. These controls result from interactions among genetic effects, organizational effects of reproductive hormones (i.e., permanent early developmental effects), and activational effects of these hormones (i.e., effects dependent on hormone levels). Male-female sex differences in the physiology of eating involve both organizational and activational effects of androgens and estrogens. An activational effect of estrogens decreases eating 1) during the periovulatory period of the ovarian cycle in rats, mice, monkeys, and women and 2) tonically between puberty and reproductive senescence or ovariectomy in rats and monkeys, sometimes in mice, and possibly in women. Estrogens acting on estrogen receptor-␣ (ER␣) in the caudal medial nucleus of the solitary tract appear to mediate these effects in rats. Androgens, prolactin, and other reproductive hormones also affect eating in rats. Sex differences in eating are mediated by alterations in orosensory capacity and hedonics, gastric mechanoreception, ghrelin, CCK, glucagon-like peptide-1 (GLP-1), glucagon, insulin, amylin, apolipoprotein A-IV, fatty-acid oxidation, and leptin. The control of eating by central neurochemical signaling via serotonin, MSH, neuropeptide Y, Agouti-related peptide (AgRP), melanin-concentrating hormone, and dopamine is modulated by HPG function. Finally, sex differences in the physiology of eating may contribute to human obesity, anorexia nervosa, and binge eating. The variety and physiological importance of what has been learned so far warrant intensifying basic, translational, and clinical research on sex differences in eating.neuroendocrinology; estrogens; testosterone; eating disorders; obesity SEX DIFFERENCES ARE PERVASIVE in physiology and medicine (51,64,73,109,110,466,797,826). The controls of eating and energy homeostasis are no exceptions. It was observed approximately 100 years ago that removal of the ovaries leads to marked accretion of adipose tissue in rats (697), that daily food intake expressed as kilocalories per gram body weight differs between male and female rats (778), and that food intake varies regularly through the ovarian cycle in intact female rats (674, 779). Sex differences in eating have been the subject of physiological research ever since. The clinical relevance of this work is increasingly evident. In the United States, women are approximately threefold more vulnerable than men to psychiatric eating disorders (346,351) and approximately twofold more vulnerable to severe and morbid obesity (BMI Ն 35 and 40 kg/m 2 , respectively, mass/height 2 ) (226). Women also appear to suffer more from these disorders in terms of physical and psychological functioning and quality of life (24,84,273,292,465,531,762). The increased obesity burden suffered by women is reflected in the fact that Ͼ80% of bariatric surgery patients in the U...

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Section: Physiological Sex Differences In Disordered Eating)mentioning

confidence: 99%

Sex differences in the physiology of eating

Asarian

Geary²

2013

American Journal of Physiology-Regulatory, Integrative and Comp

408

349

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“…[32] [33], therefore, one cannot exclude the role of AR in sperm apoptosis. Interestingly, presence of AR transcript in mature human sperm and AR protein in both X-and Y-carrier haploid spermatozoa has been shown [34].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Steroid Receptors mRNA Fingerprints in Two Groups of Normozoospermic Patients: Men from Unexplained Infertility Couples vs. Men from Couples with Tubal Factor Infertility

Jarząbek¹,

Mikucka-Niczyporuk²,

Bielawski³

et al. 2017

OJOG

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The study of sperm cellular components at molecular level is crucial for the diagnosis of male unexplained infertility. The aim of the study was to compare the molecular profile of steroid receptors and aromatase in spermatozoa obtained from two normozoospermic groups of patients issued from couples treated for infertility. We investigated 46 male patients from unexplained infertility couples and from men, 38 where female partners presented with tubal infertility. Sperm ERs (estrogen receptors: alpha and beta), GPER (G proteincoupled estrogen receptor), AR (androgen receptor) and aromatase mRNA expression levels by TaqMan qPCR were analyzed. AR transcript level was significantly lower in sperm of men from unexplained infertility couples vs. men from couples with tubal factor infertility (P = 0.04). Although the AR mRNA expression level did not had any effect on embryo development and its implantation, a significant correlation between AR mRNA levels and clinical pregnancy in unexplained infertility patients was observed. Taken together, AR transcript presence in ejaculated spermatozoa could be a potential marker for unexplained infertility.

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“…Previously, we showed that radiation damage to the somatic elements of the LBNF 1 rat testes, not the spermatogonia, was responsible for this block [26]. The reversal of this block by suppression of testosterone is further evidence that the somatic cells are responsible [1], because the germ cells do not express androgen receptor. The further restoration of spermatogonial differentiation by additional E2 treatment [3] can also be a result of action on somatic cells, because the Leydig cells and, likely, the Sertoli and peritubular cells contain estrogen receptors [5].…”

Section: Introductionmentioning

confidence: 87%

“…During studies of regulation of spermatogenic recovery in rats after gonadotoxic therapy for cancer, we found that estrogen stimulated the recovery of spermatogonial differentiation [1][2][3], but the mechanism of action was not identified. Estrogens indeed have widespread effects on spermatogenesis and male reproduction, but those effects and the mechanisms involved are quite complex [4,5].…”

Section: Introductionmentioning

confidence: 97%

Estrogen Regulated Genes in Rat Testes and Their Relationship to Recovery of Spermatogenesis after Irradiation.

Zhou

Bolden-Tiller

Shao

et al. 2011

Biology of Reproduction

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Despite numerous observations of the effects of estrogens on spermatogenesis, identification of estrogen-regulated genes in the testis is limited. Using rats in which irradiation had completely blocked spermatogonial differentiation, we previously showed that testosterone suppression with gonadotropinreleasing hormone-antagonist acyline and the antiandrogen flutamide stimulated spermatogenic recovery and that addition of estradiol (E2) to this regimen accelerated this recovery. We report here the global changes in testicular cell gene expression induced by the E2 treatment. By minimizing the changes in other hormones and using concurrent data on regulation of the genes by these hormones, we were able to dissect the effects of estrogen on gene expression, independent of gonadotropin or testosterone changes. Expression of 20 genes, largely in somatic cells, was up-or downregulated between 2-and 5-fold by E2. The unexpected and striking enrichment of transcripts not corresponding to known genes among the E2-downregulated probes suggested that these might represent noncoding mRNAs; indeed, we have identified several as miRNAs and their potential target genes in this system. We propose that genes for which expression levels are altered in one direction by irradiation and in the opposite direction by both testosterone suppression and E2 treatment are candidates for controlling the block in differentiation. Several genes, including insulin-like 3 (Insl3), satisfied those criteria. If they are indeed involved in the inhibition of spermatogonial differentiation, they may be candidate targets for treatments to enhance recovery of spermatogenesis following gonadotoxic exposures, such as those resulting from cancer therapy.

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Inhibition of Recovery of Spermatogenesis in Irradiated Rats by Different Androgens

Cited by 52 publications

References 47 publications

Sex differences in the physiology of eating

Sex differences in the physiology of eating

Evaluation of Steroid Receptors mRNA Fingerprints in Two Groups of Normozoospermic Patients: Men from Unexplained Infertility Couples vs. Men from Couples with Tubal Factor Infertility

Estrogen Regulated Genes in Rat Testes and Their Relationship to Recovery of Spermatogenesis after Irradiation.

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