Maternal protein restriction in pregnancy and/or lactation affects seminiferous tubule organization in male rat offspring

2012 ◽  
Vol 3 (5) ◽  
pp. 321-326 ◽  
Author(s):  
G. L. Rodríguez-González ◽  
R. M. Vigueras-Villaseñor ◽  
S. Millán ◽  
N. Moran ◽  
R. Trejo ◽  
...  
Keyword(s):  
Body Weight ◽  
Germ Cell ◽  
Control Diet ◽  
Protein Restriction ◽  
Male Offspring ◽  
Male Rat ◽  
Testis Weight ◽  
Germ Cell Differentiation ◽  
Maternal Protein Restriction ◽  
Cell Proliferation And Differentiation

Maternal protein restriction (MPR) during pregnancy impaired the reproduction of male offspring. We investigated, during the first wave of spermatogenesis, whether MPR exerts deleterious effects on germ cell proliferation and differentiation, as well as androgen receptor (AR) protein expression, which was used as a marker for Sertoli cell (SC) maturation. At the beginning of pregnancy (day 0), dams were fed a control diet (C: 20% casein) or a restricted isocaloric diet (R: 10% casein). After birth, four groups were established: CC, RR, CR and RC (first letter diet during pregnancy and second during lactation). Male offspring were studied at postnatal days 14, 21 and 36. At birth, pup body weight was unchanged. Body weight and testis weight were reduced in RR and CR groups at all ages evaluated. MPR delayed the germinal epithelium development at all ages evaluated. On performing Western blot and immunohistochemistry, AR expression was found to be lower in the three restricted groups. The results suggest that MPR during pregnancy and/or lactation delays SC maturation and germ cell differentiation, and affects intratubular organization. These changes might be responsible for the lower fertility rate at older ages.

The impact of maternal protein restriction during perinatal life on the response to a septic insult in adult rats

2020 ◽  
pp. 1-8
Author(s):  
Reza Khazaee ◽  
Anastasiya Vinokurtseva ◽  
Lynda A. McCaig ◽  
Cory Yamashita ◽  
Daniel B. Hardy ◽  
...  
Keyword(s):  
Control Diet ◽  
Protein Restriction ◽  
Saline Control ◽  
Female Adult ◽  
Adult Rats ◽  
Male And Female ◽  
Maternal Protein Restriction ◽  
And Control ◽  
The Impact ◽  
Septic Insult

Abstract Although abundant evidence exists that adverse events during pregnancy lead to chronic conditions, there is limited information on the impact of acute insults such as sepsis. This study tested the hypothesis that impaired fetal development leads to altered organ responses to a septic insult in both male and female adult offspring. Fetal growth restricted (FGR) rats were generated using a maternal protein-restricted diet. Male and female FGR and control diet rats were housed until 150–160 d of age when they were exposed either a saline (control) or a fecal slurry intraperitoneal (Sepsis) injection. After 6 h, livers and lungs were analyzed for inflammation and, additionally, the amounts and function of pulmonary surfactant were measured. The results showed increases in the steady-state mRNA levels of inflammatory cytokines in the liver in response to the septic insult in both males and females; these responses were not different between FGR and control diet groups. In the lungs, cytokines were not detectable in any of the experimental groups. A significant decrease in the relative amount of surfactant was observed in male FGR offspring, but this was not observed in control males or in female animals. Overall, it is concluded that FGR induced by maternal protein restriction does not impact liver and lung inflammatory response to sepsis in either male or female adult rats. An altered septic response in male FGR offspring with respect to surfactant may imply a contribution to lung dysfunction.

Maternal treatment with fluoxetine promotes testicular alteration in male rat pups

2016 ◽  
Vol 28 (8) ◽  
pp. 1206 ◽  
Author(s):  
Aline C. Ramos ◽  
Alice H. dos Santos ◽  
Kennia M. Silveira ◽  
Ana Carolina I. Kiss ◽  
Suzana F. P. Mesquita ◽  
...  
Keyword(s):  
Tap Water ◽  
Post Partum ◽  
Gonadosomatic Index ◽  
Male Offspring ◽  
Male Rat ◽  
Control Group ◽  
Maternal Behaviour ◽  
Testis Weight ◽  
Water Control ◽  
Maternal Treatment

Fluoxetine (FLX) is a selective serotonin reuptake inhibitor (SSRI) antidepressant commonly prescribed during pregnancy and lactation. Pre- and post-partum depression, as well as SSRI treatment during these periods, may change maternal care, interfering with offspring development. Moreover, it is known that SSRIs may alter testes structure and function in offspring. The present study investigated the effects of maternal FLX exposure on maternal behaviour and testes function in offspring. Female Wistar rats were treated with 7.5 mg kg–1 FLX or tap water (control group) by gavage from the Day 1 of pregnancy until 21 days after birth (postnatal Day (PND) 21). Maternal behaviour was evaluated and morphofunctional analyses of offspring testes were conducted on PND 21 and 50. There were no significant differences between the FLX-treated and control groups regarding maternal behaviour. Nor did maternal treatment with FLX have any effect on bodyweight gain, anogenital distance, day of preputial separation, testis weight and the gonadosomatic index in male offspring. However, there was a decreased number of Sertoli cells at both PND 21 and 50 in FLX-exposed male offspring. The findings of the present study demonstrate that maternal exposure to FLX can impair testicular function in weanling and pubertal animals.

scholarly journals Long-Term Effects of Maternal Low-Protein Diet and Post-weaning High-Fat Feeding on Glucose Metabolism and Hypothalamic POMC Promoter Methylation in Offspring Mice

2021 ◽  
Vol 8 ◽  
Author(s):  
Jia Zheng ◽  
Ling Zhang ◽  
Jiayi Liu ◽  
Yanli Li ◽  
Junqing Zhang
Keyword(s):  
Glucose Metabolism ◽  
Critical Role ◽  
Protein Restriction ◽  
Male Offspring ◽  
Melanocortin Receptor ◽  
High Fat ◽  
Altered Expression ◽  
Low Protein ◽  
Maternal Protein Restriction ◽  
Fat Feeding

Substantial evidence indicated that maternal malnutrition could increase the susceptibility to obesity, insulin resistance, and type 2 diabetes in adulthood. It is increasingly apparent that the brain, especially the hypothalamus, plays a critical role in glucose homeostasis. However, little information is known about the mechanisms linking maternal protein restriction combined with post-weaning high-fat (HF) feeding with altered expression of brain neurotransmitters, and investigations into the epigenetic modifications of hypothalamus in offspring have not been fully elucidated. Our objective was to explore the effects of maternal protein restriction combined with post-weaning HF feeding on glucose metabolism and hypothalamic POMC methylation in male offspring mice. C57/BL6 mice were fed on either low-protein (LP) or normal chow (NC) diet throughout gestation and lactation. Then, the male offspring were randomly weaned to either NC or high-fat (HF) diet until 32 weeks of age. Gene expressions and DNA methylation of hypothalamic proopiomelanocortin (POMC) and melanocortin receptor 4 (MC4R) were determined in male offspring. The results showed that birth weights and body weights at weaning were both significantly lower in male offspring mice of the dams fed with a LP diet. Maternal protein restriction combined with post-weaning high-fat feeding, predisposes higher body weight, persistent glucose intolerance (from weaning to 32 weeks of age), hyperinsulinemia, and hyperleptinemia in male offspring mice. POMC and MC4R expressions were significantly increased in offspring mice fed with maternal LP and postnatal high-fat diet (P < 0.05). Furthermore, maternal protein restriction combined with post-weaning high-fat feeding induced hypomethylation of POMC promoter in the hypothalamus (P < 0.05) and POMC-specific methylation (%) was negatively correlated with the glucose response to a glucose load in male offspring mice (r = −0.42, P = 0.039). In conclusion, maternal LP diet combined with post-weaning high-fat feeding predisposed the male offspring to impaired glucose metabolism and hypothalamic POMC hypomethylation. These findings can advance our thinking about hypothalamic POMC gene methylation between maternal LP diet combined with post-weaning high-fat feeding and metabolic health in offspring.

An early fish oil-enriched diet reverses biochemical, liver and adipose tissue alterations in male offspring from maternal protein restriction in mice

2011 ◽  
Vol 22 (11) ◽  
pp. 1009-1014 ◽  
Author(s):  
Isabele Bringhenti ◽  
Alini Schultz ◽  
Tamiris Rachid ◽  
Marco A. Bomfim ◽  
Carlos A. Mandarim-de-Lacerda ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fish Oil ◽  
Protein Restriction ◽  
Male Offspring ◽  
Maternal Protein Restriction ◽  
Tissue Alterations

scholarly journals The rapamycin analog Everolimus reversibly impairs male germ cell differentiation and fertility in the mouse†

2020 ◽  
Vol 103 (5) ◽  
pp. 1132-1143
Author(s):  
Oleksandr Kirsanov ◽  
Randall H Renegar ◽  
Jonathan T Busada ◽  
Nicholas D Serra ◽  
Ellen V Harrington ◽  
...  
Keyword(s):  
Body Weight ◽  
Negative Impact ◽  
Transplant Rejection ◽  
Recovery Period ◽  
Mammalian Target Of Rapamycin ◽  
Organ Transplant ◽  
Testis Weight ◽  
Adult Mice ◽  
Germ Cell Differentiation ◽  
Dose Dependent

Abstract Sirolimus, also known as rapamycin, and its closely related rapamycin analog (rapalog) Everolimus inhibit “mammalian target of rapamycin complex 1” (mTORC1), whose activity is required for spermatogenesis. Everolimus is Food and Drug Administration approved for treating human patients to slow growth of aggressive cancers and preventing organ transplant rejection. Here, we test the hypothesis that rapalog inhibition of mTORC1 activity has a negative, but reversible, impact upon spermatogenesis. Juvenile (P20) or adult (P>60) mice received daily injections of sirolimus or Everolimus for 30 days, and tissues were examined at completion of treatment or following a recovery period. Rapalog treatments reduced body and testis weights, testis weight/body weight ratios, cauda epididymal sperm counts, and seminal vesicle weights in animals of both ages. Following rapalog treatment, numbers of differentiating spermatogonia were reduced, with concomitant increases in the ratio of undifferentiated spermatogonia to total number of remaining germ cells. To determine if even low doses of Everolimus can inhibit spermatogenesis, an additional group of adult mice received a dose of Everolimus ∼6-fold lower than a human clinical dose used to treat cancer. In these animals, only testis weights, testis weight/body weight ratios, and tubule diameters were reduced. Return to control values following a recovery period was variable for each of the measured parameters and was duration and dose dependent. Together, these data indicate rapalogs exerted a dose-dependent restriction on overall growth of juvenile and adult mice and negative impact upon spermatogenesis that were largely reversed; following treatment cessation, males from all treatment groups were able to sire offspring.

scholarly journals Impacts of obesity, maternal obesity and nicotinamide mononucleotide supplementation on sperm quality in mice

Reproduction ◽  
2019 ◽  
Vol 158 (2) ◽  
pp. 171-181 ◽  
Author(s):  
Neil A Youngson ◽  
G Mezbah Uddin ◽  
Abhirup Das ◽  
Carl Martinez ◽  
Haley S Connaughton ◽  
...  
Keyword(s):  
Body Weight ◽  
Maternal Obesity ◽  
Sperm Quality ◽  
Sperm Count ◽  
Control Diet ◽  
Male Offspring ◽  
Sperm Chromatin ◽  
Sperm Dna Fragmentation ◽  
Female Mice ◽  
Nicotinamide Mononucleotide

Male fertility and sperm quality are negatively impacted by obesity. Furthermore, recent evidence has shown that male offspring from obese rat mothers also have reduced sperm quality and fertility. Here, we extend work in this area by comparing the effects of both maternal obesity and offspring post-weaning diet-induced obesity, as well as their combination, on sperm quality in mice. We additionally tested whether administration of the NAD+-booster nicotinamide mononucleotide (NMN) can ameliorate the negative effects of obesity and maternal obesity on sperm quality. We previously showed that intraperitoneal (i.p.) injection of NMN can reduce the metabolic deficits induced by maternal obesity or post-weaning dietary obesity in mice. In this study, female mice were fed a high-fat diet (HFD) for 6 weeks until they were 18% heavier than a control diet group. Thereafter, HFD and control female mice were mated with control diet males, and male offspring were weaned into groups receiving control or HFD. At 30 weeks of age, mice received 500 mg/kg body weight NMN or vehicle PBS i.p. for 21 days. As expected, adiposity was increased by both maternal and post-weaning HFD but reduced by NMN supplementation. Post-weaning HFD reduced sperm count and motility, while maternal HFD increased offspring sperm DNA fragmentation and levels of aberrant sperm chromatin. There was no evidence that the combination of post-weaning and maternal HFD exacerbated the impacts in sperm quality suggesting that they impact spermatogenesis through different mechanisms. Surprisingly NMN reduced sperm count, vitality and increased sperm oxidative DNA damage, which was associated with increased NAD+ in testes. A subsequent experiment using oral NMN at 400 mg/kg body weight was not associated with reduced sperm viability, oxidative stress, mitochondrial dysfunction or increased NAD+ in testes, suggesting that the negative impacts on sperm could be dependent on dose or mode of administration.

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