Neonatal lipopolysaccharide exposure impairs sexual development and reproductive success in the Wistar rat.

We investigated, in rats, whether neonatal exposure to bacterial lipopolysaccharide (LPS) impairs sexual development, sexual decline, and reproductive behaviour in later life. Rats were administered either LPS (Salmonella enterica, serotype enteritidis, 0.05 mg/kg, ip) or saline (equivolume) on days 3 and 5 postpartum. The immediate and long-term effect of treatment on HPA and HPG hormones, testicular morphology, and mating behaviour was assessed. Neonatal LPS exposure induced a significant increase in corticosterone compared to controls, as well as reduced testosterone and LH in males and LH in females immediately following neonatal drug exposure. Neonatal LPS exposure disrupted the normal weight-to-age ratio of puberty onset in males and females, and impaired sexual performance in adulthood. Reproductive function was reflected in significantly diminished sperm presence in rats that had received neonatal LPS. LPS-treated females exhibited LH suppression during puberty, and males demonstrated testosterone suppression in late adulthood. Testosterone and LH surges during mating were significantly reduced in adult offspring treated with LPS as neonates. Furthermore, animals exposed to neonatal LPS and subsequent stress in adulthood, exhibited significantly blunted corticosterone responses. Morphometric assessment of testes taken from neonates revealed reduced gonocyte genesis immediately following LPS exposure and increased seminiferous disorganisation of the epithelium in these animals in adulthood. This research demonstrates the long-term impact of neonatal bacterial exposure on reproductive success given that early life exposure to bacteria disrupted puberty onset and sexual performance. Associated changes in neuroendocrine functioning suggest a possible mechanism through which a subfertile phenotype may arise.

[Experiment on the sexual virility of immature mice immunized with LHRH fusion protein vaccine].

OBJECTIVE: To observe the sexual virility of immature immature male mice were divided into a pre-ablactation group (n 10). The first two groups were immunized with the LHRH fusion proportion of pregnant female mice, the morphological and histological examined to conform the emasculating effect of the vaccine. When ted with testosterone (1.0 ml each) , the post-ablactation ones were rameters. RESULTS: The sexual virility of the immature mice immunized in 3 -4 months. CONCLUSION: The LHRH fusion protein vaccine mice after ablactation, and the sexual virility can recover in the pre-ablactation decrease.

Lifecourse infectious origins of sexual inequalities in central adiposity.

BACKGROUND: Social disparities in obesity are often more marked among women than men, possibly due to social factors. Taking a life-history perspective, we hypothesized that childhood infections could be relevant via sex-specific effects of immune system activation on sexual development and, hence, body shape. METHODS: We used multivariable linear regression to assess the sex-specific, adjusted associations of 'childhood' pathogens [0 (n = 1002), 1 (n = 2199), 2 (n = 3442) or 3 (n = 4833) of HSV1, CMV and hepatitis A antibodies] and 'adult' pathogens [0 (n = 5836), 1 (n = 3018) or ≥ 2 (n = 720) of HSV2, HHV8 and hepatitis B or C) with waist-hip ratio (WHR) and body mass index (BMI) standard deviations (SDs) using NHANES III (1988-94). As validation, we assessed associations with height. RESULTS: 'Childhood' pathogens were positively associated with WHR among women [0.18 SD, 95% confidence interval (95% CI) 0.04-0.32 for 3, compared with 0], but not men (-0.04 SD, 95% CI -0.15 to 0.08), adjusted for age, education, race/ethnicity, smoking and alcohol. Further adjustments for leg length barely changed the estimates. There were no such sex-specific associations for BMI or for adult pathogens. 'Childhood', but not 'adult', pathogens were negatively associated with height, adjusted for age, sex, education and race/ethnicity. CONCLUSIONS: These observations are consistent with the lifecourse hypothesis that early exposure to infections makes women vulnerable to central obesity. This hypothesis potentially sheds new light on the developmental origins of obesity, and is consistent with the generally higher levels of central obesity among women than men in developing populations.