Prepubertal onset of obesity negatively impacts on testicular steroidogenesis in rats

Wagner, Isabel; Klöting, Nora; Atanassova, Nina; Savchuk, Iuliia; Spröte, C.; Kieß, Wieland; Söder, Olle; Svechnikov, Konstantin

doi:10.1016/j.mce.2016.08.027

Cited by 28 publications

(20 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This can be caused by the reduced intratesticular levels of leptin or the decreased sensitivity of testicular cells to this adipokine that participates in the regulation of survival and proliferation of Leydig cells (Figure 1). Although the plasma T level in obese male rats did not change, in the testes of animals it decreased by 25%, which was associated with a decrease in the expression of the Star and Cyp11a1 genes encoding StAR and cytochrome P450 scc [105].…”

Section: Leptin Regulation Of the Male Gonadal Axis And Steroidogenesmentioning

confidence: 84%

The Regulation of the Male Hypothalamic-Pituitary-Gonadal Axis and Testosterone Production by Adipokines

Шпаков¹,

Ryzhov²,

Bakhtyukov³

et al. 2018

Advances in Testosterone Action

View full text Add to dashboard Cite

There is evidence that the mass and metabolic status of the adipose tissue that produces adipokines significantly affect the activity of the hypothalamic-pituitary-gonadal (HPG) axis and the synthesis of testosterone. This is due to the fact that adipokines, such as leptin, adiponectin, visfatin and resistin have an important role in the regulation of the male HPG axis and steroidogenesis in the testes. The regulation of the HPG axis by adipokines can be carried out both through the changes the plasma levels of adipokines (a systemic regulation) and through the changes in the expression and activity of adipokines in the pituitary and testes, the components of the HPG axis (an autonomous regulation). This review presents the comprehensive analysis of the involvement of leptin, adiponectin, resistin and visfatin in the regulation of the male HPG axis and the testosterone production, as well as of the possible mechanisms of this regulation. The role of adipokines in the dysregulation of the male reproductive system and the impaired steroidogenic activity in the testes in obesity and type 2 diabetes mellitus are also discussed.

show abstract

Section: Leptin Regulation Of the Male Gonadal Axis And Steroidogenesmentioning

confidence: 84%

The Regulation of the Male Hypothalamic-Pituitary-Gonadal Axis and Testosterone Production by Adipokines

Шпаков¹,

Ryzhov²,

Bakhtyukov³

et al. 2018

Advances in Testosterone Action

View full text Add to dashboard Cite

show abstract

“…5A–C , n = 5). Since inflammatory cytokines have been found to be induced by chronic stress in testes 49 and also play a vital role in the regulation of iNOS 50 , we further evaluated the level of TNF-α in serum in different group and investigated the effect of melatonin. The level of TNF-α was increased in the stressed group (0.353 ± 0.054 pg/mg protein vs .…”

Section: Resultsmentioning

confidence: 99%

Melatonin ameliorates restraint stress-induced oxidative stress and apoptosis in testicular cells via NF-κB/iNOS and Nrf2/ HO-1 signaling pathway

Guo

Sun

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Decline in semen quality has become a global public health concern. Psychological stress is common in the current modern society and is associated with semen decline. Increasing evidence demonstrated that melatonin has anti-apoptotic and antioxidant functions. Whether melatonin can ameliorate the damage in testes induced by psychological stress has never been investigated. Here, a mouse model of restraint stress demonstrated that melatonin normalized the sperm density decline, testicular cells apoptosis, and testicular oxidative stress in stressed male mice. Melatonin decreased reactive oxygen species (ROS) level, increased superoxide dismutase (SOD) and glutathione (GSH) activities, and downregulated inducible nitric oxide synthase (iNOS) and tumor necrosis factor-α (TNF-α) activities in stressed mice testes. Furthermore, melatonin reduced the stress-induced activation of the NF-κB signaling pathway by decreasing the phosphorylation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) and p65 nuclear translocation. In addition, melatonin upregulated the expression of anti-oxidant proteins including nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). Meanwhile, in vitro studies also demonstrated melatonin could reduce oxidative apoptosis of testicular cells. Collectively, melatonin mitigated psychological stress-induced spermatogenic damage, which provides evidence for melatonin as a therapy against sperm impairment associated with psychological stress.

show abstract

“…Furthermore, impaired fertility markers and reduced reproductive functions have been observed both in obese humans and in animal models of obesity [80, 81]. Leptin-deficient mice have central hypogonadism and hence show reduced fertility.…”

Section: Obesity and Pubertal Onset And Progressionmentioning

confidence: 99%

Putative Effects of Obesity on Linear Growth and Puberty

Shalitin

Kieß²

2017

Horm Res Paediatr

View full text Add to dashboard Cite

Childhood obesity is a major public health problem that has grown to epidemic proportions throughout the world. Obesity is influenced by genetic and environmental factors. The nutritional status plays an important role in growth and body weight regulation. Excess adiposity during childhood can affect the process of growth and puberty. Obese children are frequently tall for their age, with accelerated epiphyseal growth plate maturation despite low growth hormone levels. Several regulatory hormones may affect the process of linear growth in the constellation of obesity, as high levels of insulin and leptin are observed in obese children. Leptin can act as a skeletal growth factor, with a direct effect on skeletal growth centers. The finding that overweight children, especially girls, tend to mature earlier than lean children has led to the hypothesis that the degree of body fatness may trigger the neuroendocrine events that lead to the onset of puberty. Leptin receptors have been identified in the hypothalamus, as well as in gonadotrope cells, ovarian follicular cells, and Leydig cells. The increased leptin and androgen levels seen in obese children may be implicated in their earlier onset of puberty and accelerated pubertal growth. This review is focused on the interaction between childhood obesity and growth and pubertal processes.

show abstract

Prepubertal onset of obesity negatively impacts on testicular steroidogenesis in rats

Cited by 28 publications

References 37 publications

The Regulation of the Male Hypothalamic-Pituitary-Gonadal Axis and Testosterone Production by Adipokines

The Regulation of the Male Hypothalamic-Pituitary-Gonadal Axis and Testosterone Production by Adipokines

Melatonin ameliorates restraint stress-induced oxidative stress and apoptosis in testicular cells via NF-κB/iNOS and Nrf2/ HO-1 signaling pathway

Putative Effects of Obesity on Linear Growth and Puberty

Contact Info

Product

Resources

About