| Autor: |
Menezes ACF; State University of Londrina, Biological Sciences Centre, Department of General Biology, Laboratory of Toxicology and Metabolic Disorders of Reproduction, Londrina, Brazil., Wunderlich ALM; Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Brazil., Luiz KG; State University of Londrina, Biological Sciences Centre, Department of General Biology, Laboratory of Toxicology and Metabolic Disorders of Reproduction, Londrina, Brazil., Frigoli GF; State University of Londrina, Biological Sciences Centre, Department of General Biology, Laboratory of Toxicology and Metabolic Disorders of Reproduction, Londrina, Brazil., Costa IRD; State University of Londrina, Biological Sciences Centre, Department of General Biology, Laboratory of Toxicology and Metabolic Disorders of Reproduction, Londrina, Brazil., Stopa LRDS; Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Brazil., Souza CF; Multicentre Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Brazil., Guergolette RP; Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Brazil., Shishido PK; Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Brazil., Aquino ABO; Department of Physiological Sciences, State University of Londrina, Londrina, Brazil., Forcato S; Multicentre Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Brazil., Gerardin DCC; Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Brazil.; Multicentre Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Brazil.; Department of Physiological Sciences, State University of Londrina, Londrina, Brazil., Zaia CTBV; Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Brazil.; Multicentre Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Brazil.; Department of Physiological Sciences, State University of Londrina, Londrina, Brazil., Uchoa ET; Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Brazil.; Multicentre Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Brazil.; Department of Physiological Sciences, State University of Londrina, Londrina, Brazil., Fernandes GSA; State University of Londrina, Biological Sciences Centre, Department of General Biology, Laboratory of Toxicology and Metabolic Disorders of Reproduction, Londrina, Brazil.; Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Brazil. |
| Abstrakt: |
Several models of maternal undernutrition reveal impairment of testicular development and compromise spermatogenesis in male offspring. The expansion of the litter size model, valuable for studying the impact of undernutrition on early development, has not yet been used to evaluate the consequences of early undernutrition in the adult male reproductive system. For this purpose, pups were raised in either normal litter (ten pups/dam) or large litter (LL; sixteen pups/dam). On postnatal day 90, sexual behaviour was evaluated or blood, adipose and reproductive tissues were collected for biochemical, histological and morphological analysis. Adult LL animals were lighter and thinner than controls. They showed increased food intake, but decrease of retroperitoneal white adipose tissue weight, glycaemia after oral glucose overload and plasma concentration of cholesterol. Reproductive organ weights were not altered by undernutrition, but histopathological analysis revealed an increased number of abnormal seminiferous tubules and number of immature spermatids in the tubular lumen of LL animals. These animals also showed reduction in total spermatic reserve and daily sperm production in the testes. Undernutrition decreased the number of Sertoli cells, and testosterone production was increased in the LL group. Mitochondrial activity of spermatozoa remained unchanged between experimental groups, suggesting no significant impact on the energy-related processes associated with sperm function. All animals from both experimental groups were considered sexually competent, with no significant difference in the parameters of sexual behaviour. We conclude that neonatal undernutrition induces histological and physiological testicular changes, without altering sperm quality and sexual behaviour of animals. |
