Implications of leptin in neuroendocrine regulation of male reproduction

Landry, David; Cloutier, Frank; Martin, Luc J.

doi:10.1016/j.repbio.2012.12.001

Cited by 90 publications

(59 citation statements)

References 173 publications

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“…Besides, this obesity model results in insulin resistance (Ribeiro et al 2012). As testicular development and function are influenced by the insulin signaling pathway (Nef et al 2003) and leptin (Landry et al 2013), they should also be implicated in the transient alterations here described. Other experiments are underway in our laboratory to evaluate the contribution of changes in aromatase expression and insulin signaling in testis development alterations induced by MO.…”

Section: Discussionmentioning

confidence: 80%

Maternal obesity disturbs the postnatal development of gonocytes in the rat without impairment of testis structure at prepubertal age

Christante¹,

Taboga²,

Pinto-Fochi³

et al. 2013

Reproduction

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In this study, we evaluated whether maternal obesity (MO) affects testis development and gonocyte differentiation in the rat from 0.5 to 14.5 postnatal days. Male Wistar rats were used at 0.5, 4.5, 7.5, and 14.5 days post partum (dpp). These rats were born from obese mothers, previously fed with a high-fat diet (20% saturated fat), for 15 weeks, or normal mothers that had received a balanced murine diet (4% lipids). MO did not affect testis weight or histology at birth but changed the migratory behavior of gonocytes. The density of relocated cells was higher in MO pups at 0.5 dpp, decreased at 4.5 dpp, and differed from those of control pups, where density increased exponentially from 0.5 to 7.5 dpp. The numerical density of gonocytes within seminiferous cords did not vary in MO, in relation to control neonates, for any age considered, but the testis weight was 50% lower at 4.5 dpp. A wide variation in plasmatic testosterone and estrogen levels was observed among the groups during the first week of age and MO pups exhibited higher steroid concentrations at 4.5 dpp, in comparison with controls. At this age, higher estrogen levels of MO pups impaired the gonocyte proliferation. At 7.5 dpp, the testicular size and other parameters of gonocyte development are retrieved. In conclusion, MO and saturated lipid diets disturb gonocyte development and sexual steroid levels during the first days of life, with recovery at prepubertal age.

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Section: Discussionmentioning

confidence: 80%

Maternal obesity disturbs the postnatal development of gonocytes in the rat without impairment of testis structure at prepubertal age

Christante¹,

Taboga²,

Pinto-Fochi³

et al. 2013

Reproduction

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“…In addition, studies in testes of elderly rats have shown an increase in ROS levels, a reduction in StAR and a decrease in testosterone (Allen et al 2004). There is evidence which indicates that male obesity negatively impacts reproductive capacity not only by reducing sperm quality but also by affecting germ cells and spermatozoa (Palmer et al 2012) through different mechanisms such as decreased sex hormone secretion (Aggerholm et al 2008;Cabler et al 2010), increased insulin resistance (Hammoud et al 2008), and/or due to the direct action of leptin or other hormones derived from adipocytes on testicular function (Landry et al 2013). The findings of the present study of metabolic alterations coupled to the increase in testicular OS level indicate that OS may play an important role in the etiology of the fertility problems observed in adult life of the rat offspring from nutrient-restricted mothers.…”

Section: Discussionmentioning

confidence: 99%

Accelerated aging of reproductive capacity in male rat offspring of protein-restricted mothers is associated with increased testicular and sperm oxidative stress

Rodríguez-González

Reyes-Castro

Vega

et al. 2014

AGE

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Maternal protein restriction (MPR) in pregnancy causes life course organ dysfunction, but few studies link the developmental origins of disease hypothesis to early aging. Suboptimal developmental nutrition increases oxidative stress (OS) and male infertility, damaging sperm function. We hypothesized that MPR in pregnancy accelerates age-related changes in testicular and sperm function related to both maternal diet and increased testicular OS in rat offspring. We studied male rats whose pregnant mothers ate either control (C, 20 % casein) or restricted (R, 10 % casein) isocaloric diet. After birth, mothers and offspring ate C diet. Testes were retrieved at 19 days gestation and across the life course (postnatal day (PND) 21, 36, 110, and 850) to measure OS markers, antioxidant enzymes, serum FSH, LH, and testosterone, and PND 110 sperm OS and quality. Fertility rate was evaluated at PND 110, 450, and 850. Offspring showed age-and MPRrelated changes in testosterone, testicular OS markers and antioxidant enzymes and fertility, and maternal diet-related OS and sperm antioxidant enzyme changes. Developmental programming is considered a key factor in predisposing to chronic disease. Our data show that programming also plays an important role in aging trajectory. This interaction is a little studied area in aging biology that merits more investigation. Keywords

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“…Intrinsic factors derive from genes predominantly expressed in testis, including DEAD (Asp-Glu-Ala-Asp) box polypeptide 4 (DDX4), synaptonemal complex protein 3, and deleted in azoospermia 1 among others, whereas extrinsic factors originate from the hypothalamus, pituitary gland, and other organs. Recent studies have shown that the secretion of adipokines, such as leptin from adipose tissue, regulates reproductive function by affecting the hypothalamuspituitary-gonadal (HPG) axis (1,2). Evidence for a link between adipose tissue function and male fertility has also emerged from several studies showing a negative impact of obesity on male reproduction (3,4).…”

mentioning

confidence: 99%

Lack of testicular seipin causes teratozoospermia syndrome in men

Jiang

Gao

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Obesity impairs male fertility, providing evidence for a link between adipose tissue and reproductive function; however, potential consequences of adipose tissue paucity on fertility remain unknown. Lack of s.c. fat is a hallmark of Berardinelli-Seip congenital lipodystrophy type 2 (BSCL2), which is caused by mutations in BSCL2-encoding seipin. Mice with a targeted deletion of murine seipin model BSCL2 with severe lipodystrophy, insulin resistance, and fatty liver but also exhibit male sterility. Here, we report teratozoospermia syndrome in a lipodystrophic patient with compound BSCL2 mutations, with sperm defects resembling the defects of infertile seipin null mutant mice. Analysis of conditional mouse mutants revealed that adipocyte-specific loss of seipin causes progressive lipodystrophy without affecting fertility, whereas loss of seipin in germ cells results in complete male infertility and teratozoospermia. Spermatids of the human patient and mice devoid of seipin in germ cells are morphologically abnormal with large ectopic lipid droplets and aggregate in dysfunctional clusters. Elevated levels of phosphatidic acid accompanied with an altered ratio of polyunsaturated to monounsaturated and saturated fatty acids in mutant mouse testes indicate impaired phospholipid homeostasis during spermiogenesis. We conclude that testicular but not adipose tissue-derived seipin is essential for male fertility by modulating testicular phospholipid homeostasis.

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Implications of leptin in neuroendocrine regulation of male reproduction

Cited by 90 publications

References 173 publications

Maternal obesity disturbs the postnatal development of gonocytes in the rat without impairment of testis structure at prepubertal age

Maternal obesity disturbs the postnatal development of gonocytes in the rat without impairment of testis structure at prepubertal age

Accelerated aging of reproductive capacity in male rat offspring of protein-restricted mothers is associated with increased testicular and sperm oxidative stress

Lack of testicular seipin causes teratozoospermia syndrome in men

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