Hyperleptinemia directly affects testicular maturation at different sexual stages in mice, and suppressor of cytokine signaling 3 is involved in this process

Miao, Yuan; Huang, Guizhen; Li, Jun; Zhang, Jie; Li, Fēi; Li, Kai; Gao, Bo; Zeng, Li; Shan, Wanying; Lin, Ping; Huang, Lei

doi:10.1186/1477-7827-12-15

Cited by 44 publications

(32 citation statements)

References 46 publications

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“…Leptin caused STAT 3 phosphorylation after in vitro incubation of isolated seminiferous tubules, demonstrating that Ob-R is functional and an activator of signal transduction mechanisms in germ cells ( 72 ). Corroborating this result, recently it was shown that leptin activates STAT3 signaling in the testis and that SOCS3 expression is regulated by leptin in this tissue ( 73 ).…”

Section: Leptinmentioning

confidence: 76%

Thyroid Hormone and Leptin in the Testis

Ramos

Zamoner

2014

Front. Endocrinol.

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Leptin is primarily expressed in white adipose tissue; however, it is expressed in the hypothalamus and reproductive tissues as well. Leptin acts by activating the leptin receptors (Ob-Rs). Additionally, the regulation of several neuroendocrine and reproductive functions, including the inhibition of glucocorticoids and enhancement of thyroxine and sex hormone concentrations in human beings and mice are leptin functions. It has been suggested that thyroid hormones (TH) could directly regulate leptin expression. Additionally, hypothyroidism compromises the intracellular integration of leptin signaling specifically in the arcuate nucleus. Two TH receptor isoforms are expressed in the testis, TRa and TRb, with TRa being the predominant one that is present in all stages of development. The effects of TH involve the proliferation and differentiation of Sertoli and Leydig cells during development, spermatogenesis, and steroidogenesis. In this context, TH disorders are associated with sexual dysfunction. An endocrine and/or direct paracrine effect of leptin on the gonads inhibits testosterone production in Leydig cells. Further studies are necessary to clarify the effects of both hormones in the testis during hypothyroidism. The goal of this review is to highlight the current knowledge regarding leptin and TH in the testis.

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Section: Leptinmentioning

confidence: 76%

Thyroid Hormone and Leptin in the Testis

Ramos

Zamoner

2014

Front. Endocrinol.

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“…(), authors showed that leptin inhibits testosterone, luteinizing hormone, and follicle‐stimulating hormone secretion in adult rat testis and pituitaries in vitro, indicating that the effect of leptin on the reproductive system are complex and presumably occur at various levels of the hypothalamic–pituitary–gonadal axis. A high concentration of leptin decreased a variety of reproductive parameters including the weight and volume of the testicles, the diameter of the seminiferous tubules, the numbers of the spermatocytes, spermatozoa, Leydig cells, and offspring in mice (Yuan et al ., ). On the other hand, Schoeller et al .…”

Section: Introductionmentioning

confidence: 97%

Genetic variation in leptin and leptin receptor genes as a risk factor for idiopathic male infertility

et al. 2016

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SUMMARYThe aim of this study was to examine whether there is an association among genetic variability in leptin (LEP) and leptin receptor (LEPR) genes and male infertility. We performed a case-control study and were searching for an association between polymorphisms of LEP and LEPR genes and male infertility. The study group consisted of 317 patients with idiopathic infertility and a control group of 241 fertile men from Slovenia. Four single nucleotide polymorphisms (SNPs) in LEP gene and four single nucleotide polymorphisms (SNPs) in LEPR gene were chosen and genotyped. Statistically significant SNP was further validated in additional 255 infertile patients and 168 controls from Serbia and Macedonia. In the Slovenian population, we found a statistically significant difference in genotype distribution for rs10244329 polymorphism in LEP gene (recessive genotype model, p value = 0.048). The trend toward statistically significant difference in genotype distribution for rs10244329 polymorphism was confirmed in the Serbian and Macedonian populations (p value = 0.07). Our data suggest that genetic variability in the LEP gene might be associated with male infertility warranting further confirmation and mechanistic investigations.

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“…Experimental data showed that testosterone in vitro had a direct effect on ß cells of pancreas and increased insulin synthesis leptin production is tightly coupled to insulin resistance and may play a key role in steroid biogenesis and reduced T levels (Jones & Saad, ). Leptin levels have been shown to be inversely correlated with serum T levels (Yuan et al ., ) and increased circulating leptin may be involved in the pathogenesis of Leydig cell dysfunction (Isidori et al ., ). The expression of leptin receptors in Leydig cells and the inhibition of hCG stimulated T secretion from rat Leydig cells by leptin suggest a role of this hormone in the biogenesis of testosterone.…”

Section: Discussionmentioning

confidence: 99%

Male hypogonadism and metabolic syndrome

Naifar

Rekik

Messedi³

et al. 2014

Andrologia

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The role of androgens in cardiovascular disease is still controversial in men. In this study, we investigated metabolic disorders in Tunisian hypogonadal men compared with healthy controls. Forty hypogonadal men and 80 control subjects were enrolled. Patients with a history of pre-existing panhypopituitarism, thyroid dysfunction or inflammatory disease were excluded. Glycaemia, glycated haemoglobin (HbA1c), high-sensitive C-reactive protein (hsCRP), lipid profile, insulin, testosterone and gonadotrophins were measured. Insulin resistance was assessed by homoeostasis model assessment of insulin resistance (Homa IR). Waist circumference, body mass index and blood pressure were significantly higher in patients compared with controls. Glycemia, HbA1c, fasting serum insulin and Homa IR were significantly increased among hypogonadal men. In univariate analysis, testosterone levels were inversely correlated with body mass index, waist circumference, blood pressure, glycaemia, HbA1C, insulin, Homa IR and hsCRP. In multivariate analysis including all significant variables, initial testosterone level was the only independent risk factor for developing dyslipidaemia. With logistic regression, male hypogonadism was an independent risk factor for MS (P < 0.001). We conclude that low testosterone level plays a central role in the development of metabolic syndrome. Further prospective data are required to establish the causative link.

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Hyperleptinemia directly affects testicular maturation at different sexual stages in mice, and suppressor of cytokine signaling 3 is involved in this process

Cited by 44 publications

References 46 publications

Thyroid Hormone and Leptin in the Testis

Thyroid Hormone and Leptin in the Testis

Genetic variation in leptin and leptin receptor genes as a risk factor for idiopathic male infertility

Male hypogonadism and metabolic syndrome

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