Endocrine Abstracts

Obesity incidence is increasing globally at an alarming rate, particularly amongst children and young adults. Male obesity has been linked with a reduction in sperm quality and consequently decreased fertilization rates. Seminal vesicles are considered fundamental for male fertility and though for men’s health. Vesicle seminal secretion contributes to a significant volume of seminal fluid, being extremely important for semen coagulation and sperm motility. Recent studies suggest that an obesity-inducing lifestyle combined with genetic changes can cause epigenetic mutations. Obesity-related genes (ORG) have been pointed out as causes for an overweight, suggesting that children born from obese parents could have a genetic predisposition to develop metabolic disorders. This project aimed to unveil molecular mechanisms related with the inheritance of an overweight through seminal vesicles. We hypothesized that ORG, Fat mass and obesity (FTO), Melanocortin-4 receptor (MC4R), Glucosamine-6-phosphate deaminase 2 (GNPDA2), and Transmembrane protein 18 (TMEM18) were present and could have a role in seminal vesicles and consequently in production of seminal fluid over three generations. Samples of seminal vesicle tissue were selected from mice included in the following experimental design: the first generation (F0) was divided into 3 groups (n=6 per group) according to administered diet. Mice are randomly fed after weaning with standard chow (CTRL); HFD for 200 days or transient HFD(HFDt) (60 days of HFD+140 days of standard chow). Subsequent generations (F1 and F2; 6 mice per generation) are fed with chow diet. Mice are euthanized 200 days post-weaning. RNA was extracted from the seminal vesicles of the 54 animals and used to evaluate the mRNA abundance of MC4R, FTO, GNPDA2 and TMEM18 through quantitative Polymerase Chain Reaction (qPCR) in the 3 groups of the 3 generations of mice. Early results suggest a significative abundance increase in all ORG genes analysed in generation F1 for all diet groups. We observed a tendency to increase the abundance of ORG from the F0 generation to the F1 generation and a further decrease in the F2 generation. Our results suggest that a high-fat diet is capable of causing changes in the expression of ORGs in the seminal vesicles of offspring of parents with poor eating habits. That is, HFD is capable of causing transgenerational damage that may manifest itself in children and grandchildren who may be more predisposed to obesity and possible fertility problems.