Diet-induced maternal obesity and overnutrition cause a decrease in the sperm quality of the offspring.

The present work aimed to study the changes caused by maternal obesity and overnutrition in both the quality and function of spermatozoa of the offspring. To this end, female rats received either a standard or cafeteria diet from 22 days of age until the weaning of their offspring, and the male offspring from rats fed the standard and cafeteria diet (OSD and OCD respectively) were used. Different endpoints in the offspring, as body weight, weight gain, and glycemia were recorded and the testes were removed at 60 days of age. Different spermatozoa parameters, such as mitochondrial function, functional integrity of the sperm plasma membrane, capacitation, and acrosome status, were evaluated. The OCD group was heavier than the OSD group and exhibited lower testis and epididymal indices. The OCD group also showed a decrease in the ability of the sperm tail to react in the presence of a hypoosmotic solution, deficiency in sperm mitochondrial function, a lower percentage of spermatozoa without acrosome when exposed to a capacitation medium, and a higher number of abnormal metaphases. In addition, compared with OSD, OCD rats had a higher number of TUNEL-positive cells in the histological sections of the testis, and greater presence of reactive oxygen species in the spermatozoa, evaluated by a fluorescent probe. However, the OCD group displayed lower protein levels of cytochrome c and caspase-3 in testis tissue than the control group. These results suggest that maternal obesity and overnutrition program the offspring to develop poor sperm quality and function, which may imply a condition of subfertility.