scholarly journals The onset of puberty in female mice as reflected in urinary steroids and uterine/ovarian mass: interactions of exposure to males, phyto-oestrogen content of diet, and ano-genital distance

Reproduction ◽  
2008 ◽  
Vol 135 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Ayesha Khan ◽  
Robert G Berger ◽  
Denys deCatanzaro
Keyword(s):  
In Utero ◽  
Adult Males ◽  
Ovarian Mass ◽  
Indirect Measure ◽  
Urinary Creatinine ◽  
Female Mice ◽  
Regular Diet ◽  
Urinary Steroids ◽  
Androgen Exposure

Development of puberty in female mice was examined in relationship with the ano-genital distance index (AGDI), phyto-oestrogen content of diet and exposure to males post weaning. Throughout gestation and post-natal development, females were exposed to a regular diet or a nutritionally similar diet deficient in phyto-oestrogens. After segregation at weaning on the basis of short or long AGDI, an indirect measure ofin uteroandrogen exposure, females were housed alone or underneath two outbred adult males for 2 weeks. Female urinary samples were collected non-invasively throughout this exposure, then assayed for oestradiol, progesterone and creatinine. Females were then killed and uterine and ovarian mass was determined. Urinary oestradiol was substantially reduced in females raised on the phyto-oestrogen-free diet. Oestradiol levels were more dynamic over days in urine of male-exposed females, especially among those on the regular diet. Urinary progesterone was not strongly influenced by diet. Progesterone was more dynamic in urine of male-exposed females, and was generally elevated compared with levels in isolated females, the size of this effect dependent on AGDI, diet and whether the measure was adjusted for creatinine. Urinary creatinine was elevated by the phyto-oestrogen-free diet and reduced by male exposure, tending to decline over days in females exposed to males. Male exposure increased uterine and ovarian mass and was influenced by AGDI in interaction with diet and male exposure.

Preputialectomised and intact adult male mice exhibit an elevated urinary ratio of oestradiol to creatinine in the presence of developing females, whilst promoting uterine and ovarian growth of these females

2009 ◽  
Vol 21 (7) ◽  
pp. 860 ◽  
Author(s):  
Ayesha Khan ◽  
Robert G. Berger ◽  
Denys deCatanzaro
Keyword(s):  
Sexual Maturity ◽  
Adult Males ◽  
Ovarian Mass ◽  
Reproductive Maturation ◽  
Urinary Steroids ◽  
Sham Surgery ◽  
Ovarian Growth ◽  
Uterine Growth ◽  
Preputial Glands ◽  
Female Sexual Development

Exposure to novel adult males and their urine can hasten the onset of sexual maturity in female mice. Some evidence implicates chemosignals from males’ preputial glands, while other evidence suggests that male urinary steroids, especially 17β-oestradiol, contribute to this effect. The present experiment was designed to determine whether preputial gland removal would influence the capacity of males to accelerate female sexual development, and to measure male urinary oestradiol and testosterone in the presence or absence of these glands. Juvenile females aged 28 days were housed for two weeks in isolation or underneath two outbred males that had undergone preputialectomy or sham surgery. Urine samples were collected non-invasively from males that were isolated or exposed to females, then assayed for oestradiol, testosterone and creatinine. Combined uterine and ovarian mass from females sacrificed at 43 days of age was increased by exposure to males, regardless of whether or not these males had been preputialectomised. Male urinary creatinine was reduced by exposure to developing females. Creatinine-adjusted oestradiol and testosterone were significantly greater in female-exposed than in isolated males, in both preputialectomised and intact males. These data suggest that the preputials are not necessary for the capacity of males to hasten female uterine and ovarian growth. As exogenous oestrogens can promote uterine growth and other parameters of female reproductive maturation, oestradiol in males’ urine may contribute to earlier sexual maturity in male-exposed females.

scholarly journals The Pancreas Is Altered by In Utero Androgen Exposure: Implications for Clinical Conditions Such as Polycystic Ovary Syndrome (PCOS)

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e56263 ◽  
Author(s):  
Mick Rae ◽  
Cathal Grace ◽  
Kirsten Hogg ◽  
Lisa Marie Wilson ◽  
Sophie L. McHaffie ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
In Utero ◽  
Ovary Syndrome ◽  
Androgen Exposure ◽  
Clinical Conditions

scholarly journals Prenatal androgen exposure programs metabolic dysfunction in female mice

2010 ◽  
Vol 207 (2) ◽  
pp. 213-223 ◽  
Author(s):  
Alison V Roland ◽  
Craig S Nunemaker ◽  
Susanna R Keller ◽  
Suzanne M Moenter
Keyword(s):  
Pancreatic Islet ◽  
Polycystic Ovary ◽  
Islet Function ◽  
Metabolic Dysfunction ◽  
Isolated Pancreatic Islets ◽  
Female Mice ◽  
Metabolic Characteristics ◽  
Reproductive Axis ◽  
Androgen Exposure

Polycystic ovary syndrome (PCOS) is a common fertility disorder with metabolic sequelae. Our laboratory previously characterized reproductive phenotypes in a prenatally androgenized (PNA) mouse model for PCOS. PNA mice exhibited elevated testosterone and LH levels, irregular estrous cycles, and neuroendocrine abnormalities suggesting increased central drive to the reproductive system. In this study, we examined metabolic characteristics of female PNA mice. PNA mice exhibited increased fasting glucose and impaired glucose tolerance (IGT) that were independent of age and were not associated with changes in body composition or peripheral insulin sensitivity. IGT was associated with defects in pancreatic islet function leading to an impaired response to high glucose, consistent with impaired insulin secretion. Exposure of isolated pancreatic islets to androgen in vitro demonstrated an impaired response to glucose stimulation similar to that in PNA mice, suggesting androgens may have activational in addition to organizational effects on pancreatic islet function. PNA mice also exhibited increased size of visceral adipocytes, suggesting androgen-programed differences in adipocyte differentiation and/or function. These studies demonstrate that in addition to causing reproductive axis abnormalities, in utero androgen exposure can induce long-term metabolic alterations in female mice.

scholarly journals Administration of Saccharin to Neonatal Mice Influences Body Composition of Adult Males and Reduces Body Weight of Females

Endocrinology ◽  
2014 ◽  
Vol 155 (4) ◽  
pp. 1313-1326 ◽  
Author(s):  
Sebastian D. Parlee ◽  
Becky R. Simon ◽  
Erica L. Scheller ◽  
Emilyn U. Alejandro ◽  
Brian S. Learman ◽  
...  
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Bone Mass ◽  
Composition Analysis ◽  
Male Body ◽  
Adult Males ◽  
Male Mice ◽  
Female Mice ◽  
Trabecular Bone Mass ◽  
High Concentrations

Nutritional or pharmacological perturbations during perinatal growth can cause persistent effects on the function of white adipose tissue, altering susceptibility to obesity later in life. Previous studies have established that saccharin, a nonnutritive sweetener, inhibits lipolysis in mature adipocytes and stimulates adipogenesis. Thus, the current study tested whether neonatal exposure to saccharin via maternal lactation increased susceptibility of mice to diet-induced obesity. Saccharin decreased body weight of female mice beginning postnatal week 3. Decreased liver weights on week 14 corroborated this diminished body weight. Initially, saccharin also reduced male mouse body weight. By week 5, weights transiently rebounded above controls, and by week 14, male body weights did not differ. Body composition analysis revealed that saccharin increased lean and decreased fat mass of male mice, the latter due to decreased adipocyte size and epididymal, perirenal, and sc adipose weights. A mild improvement in glucose tolerance without a change in insulin sensitivity or secretion aligned with this leaner phenotype. Interestingly, microcomputed tomography analysis indicated that saccharin also increased cortical and trabecular bone mass of male mice and modified cortical bone alone in female mice. A modest increase in circulating testosterone may contribute to the leaner phenotype in male mice. Accordingly, the current study established a developmental period in which saccharin at high concentrations reduces adiposity and increases lean and bone mass in male mice while decreasing generalized growth in female mice.

scholarly journals In utero exposure to benzo[a]pyrene increases adiposity and causes hepatic steatosis in female mice, and glutathione deficiency is protective

2013 ◽  
Vol 223 (2) ◽  
pp. 260-267 ◽  
Author(s):  
Laura Ortiz ◽  
Brooke Nakamura ◽  
Xia Li ◽  
Bruce Blumberg ◽  
Ulrike Luderer
Keyword(s):  
Hepatic Steatosis ◽  
In Utero ◽  
In Utero Exposure ◽  
Female Mice ◽  
Glutathione Deficiency

scholarly journals In utero exposure to acetaminophen and ibuprofen leads to intergenerational accelerated reproductive aging in female mice

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Moïra Rossitto ◽  
Margot Ollivier ◽  
Stéphanie Déjardin ◽  
Alain Pruvost ◽  
Christine Brun ◽  
...  
Keyword(s):  
In Utero ◽  
In Utero Exposure ◽  
Reproductive Aging ◽  
Female Mice

scholarly journals Adverse metabolic phenotype of female offspring exposed to preeclampsia in utero: a characterization of the BPH/5 mouse in postnatal life

2017 ◽  
Vol 312 (4) ◽  
pp. R485-R491 ◽  
Author(s):  
Elizabeth F. Sutton ◽  
Heinrich E. Lob ◽  
Jiunn Song ◽  
YunWei Xia ◽  
Scott Butler ◽  
...  
Keyword(s):  
Early Adulthood ◽  
Female Offspring ◽  
In Utero ◽  
Leptin Resistance ◽  
Metabolic Phenotype ◽  
Postnatal Life ◽  
Chronic Hypertension ◽  
Female Mice ◽  
Reproductive Axis ◽  
Adverse Pregnancy

Preeclampsia (PE) is a devastating disorder of pregnancy that classically presents with maternal hypertension and proteinuria after 20 wk of gestation. In addition to being a leading cause of maternal and fetal morbidity/mortality, epidemiological and prospective studies have revealed long-term consequences for both the mother and baby of preeclamptic pregnancies, including chronic hypertension as well as other cardiovascular diseases and metabolic derangements. To better understand the effect of in utero exposure of PE on offspring, we utilized the BPH/5 mouse, a spontaneous model of the maternal and fetal PE syndrome. We hypothesized that young BPH/5 offspring would have altered metabolic and cardiovascular phenotypes. Indeed, BPH/5 growth-restricted offspring showed excess catch-up growth by early adulthood due to hyperphagia and increased white adipose tissue (WAT) accumulation, with inflammation markers isolated to the reproductive WAT depot only. Both excessive WAT accumulation and the inflammatory WAT phenotype were corrected by pair-feeding young BPH/5 female mice. We also found that young BPH/5 female mice showed evidence of leptin resistance. Indeed, chronic hyperleptinemia has been shown to characterize other rodent models of PE; however, the maternal metabolic profile before pregnancy has not been fully understood. Furthermore, we found that these mice show signs of cardiovascular anomalies (hypertension and cardiomegaly) and altered signaling within the reproductive axis in early life. Future studies will involve challenging the physiological metabolic state of BPH/5 mice through pair-feeding to reduce WAT before pregnancy and determining its causal role in adverse pregnancy outcomes.

Sign in / Sign up

Export Citation Format

Share Document