Disruption in the sperm quality of the offspring caused by maternal overnutrition in rats

Abstract

Obesity has increased in recent years and is the most importantnoncommunicable chronic disease. Maternal overnutrition may inducemultiple pathologies in both women and their offspring. Ourprevious studies showed that male offspring from high-fat-fed ratsexhibited higher body and testis weight and altered puberty. Also,we found a lower number of germ cells, percentage of motile spermand capacitation. Thus, the aim of the present study was to evaluatethe effects of maternal overnutrition, induced by high-fat diet, on thequality and function of sperm in the offspring.To this end, maternalovernutrition were induced by a high-fat palatable (cafeteria) diet,which was supplied continuously until weaning of their offspring, includingpregnancy and lactation. Male offspring from rats fed standard(OSD) or cafeteria diet (OCD) were fed with a standard diet, inspectedperiodically, and euthanized at 60 days of age. In the germcells we examined the presence of the reactive oxygen species byflow cytometry using a fluorescent probe (2,7-dichlorofluorescein diacetate),DNA fragmentation by TUNEL kit, mitochondrial functionusing the probe 3.3-diaminobenzidine, the membrane functionalstatus by hypoosmotic swelling test, and the presence of abnormalchromosomes by cytogenetic assay (Evan test). Compared withOSD rats, OCD group showed a lower percentage of the hypoosmotic-reacted sperm (15±1 vs 23±2, p<0.01) and an increase in theabnormal metaphases (6±1 vs 2.1±0.7, p<0.001). No differenceswere found in the TUNEL positive cells, but OCD exhibited higherfluorescein intensity expressed as relative units (577±74, p<0.01)compared with OSD (233±27). Finally, 50% of OCD rats displayeda lower mitochondrial function, expressed as relative units (94.8±4vs 97.7±0.4 from OSD, p<0.01).These results indicate that diet-inducedmaternal overnutrition may contribute to disorders in the fetalprogramming, particularly in the germ cell quality.