Obesogenic Environment by Excess of Dietary Fats in Different Phases of Development Reduces Spermatic Efficiency of Wistar Rats at Adulthood: Correlations with Metabolic Status1

Abstract

This study compares the impact of obesogenic environment (OE) in six different periods of development on sperm parameters and the testicular structure of adult rats and their correlations with sex steroid and metabolic scenario. Wistar rats were exposed to OE during gestation (O1), during gestation/lactation (O2), from weaning to adulthood (O3), from lactation to adulthood (O4), from gestation to sexual maturity (O5), and after sexual maturation (O6). OE was induced by a 20% fat diet, and control groups were fed a balanced diet (4% fat). Serum leptin levels and adiposity index indicate that all groups were obese, except for O1. Three progressive levels of impaired metabolic status were observed: O1 presented insulin resistance, O2 were insulin resistant and obese, and groups O3, O4, and O5 were insulin resistant, obese, and diabetic. These three levels of metabolic damage were proportional to the increase of leptin and decreased circulating testosterone. The impairment in the daily sperm production (DSP) paralleled these three levels of metabolic and hormonal damage being marginal in O1, increasing in O2, and being higher in groups O3, O4, O5, and O6. None of the OE periods affected the sperm transit time in the epididymis, and the lower sperm reserves were caused mainly by impaired DSP. In conclusion, OE during sexual maturation markedly reduces the DSP at adulthood in the rat. A severe reduction in the DSP also occurs in OE exposure during gestation/lactation but not in gestation, indicating that breast-feeding is a critical period for spermatogenic impairment under obesogenic conditions.

Differential ontogenetic exposure to obesogenic environment induces hyperproliferative status and nuclear receptors imbalance in the rat prostate at adulthood

“…Therefore, our data are in agreement with literature [48][49][50][51][52] and show that a diet containing 20% of lipids is a good model for studying obesity and insulin resistance when administered for prolonged times. The metabolic scenario observed in these groups was also in accordance with recent data from our laboratory using a similar experimental design and indicated progressive levels of impairment on metabolic status [53], since the group exposed only in gestation (G) was insulin resistant, that exposed in gestation/lactation (GL) was insulin resistant and overweight, and the other (WA, LA, and GA) were insulin-resistant and obese. In addition to the metabolic scenario, this investigation shows a significant increase in periprostatic fat deposits (PP) in WA, LA, and GA groups.…”

Melatonin intake since weaning ameliorates steroidogenic function and sperm motility of streptozotocin‐induced diabetic rats

“…These authors verified that metabolic alterations modulated by testosterone decline in diabetes favored glycogen accumulation in these cells, and this may be detrimental for the metabolic support of spermatogenesis by Sertoli cells. Our team has also observed premature detachment of germ cells associated to decreased circulating testosterone in testes of rats exhibiting several features of pre‐diabetes due to prolonged feeding with high‐fat diet (Reame et al ., ). Thus, the premature detachment of developing germ cells observed here may be a consequence of metabolic alterations in Sertoli cells caused by insulin and testosterone scarcity.…”

High butter-fat diet and bisphenol A additively impair male rat spermatogenesis

“…In Sprague-Dawley (SD) rats, the testicular E2 to T ratio is highest at 18 months of age [20], coinciding with declining sperm production. Other contributors to reduced spermatogenesis include exposure to xeno/phyto-estrogens, obesity, inflammatory cytokines, poor dietary choices, and reactive toxins [21–24], all of which contribute to stress, and also increase E2 levels. Here, we have employed two models to investigate the effects of maternal exposure to BPA and high fat diets on spermatogenesis in offspring (1) a hormone treatment model in which male rats are exposed to T + E2 at postnatal day (PND)70-210 to mimic an accelerated aging process and (2) a natural aging model, where rats are sacrificed at 18 months (PND 540).…”