Background <p>An unhealthy diet contributes significantly to the development of the global obesity epidemic and serves as a risk factor for fertility disorders. Moreover, maternal obesity leads to alterations in the reproductive capacity of the offspring via prenatal and postnatal programming.</p> Methods <p>To replicate the impact of a diet rich in sugar and fat, which contributes to human obesity, we utilized a cafeteria (CAF) diet in rat mothers to investigate molecular and morphological consequences in the gonads of male and female progeny. Rat mothers were fed either standard (control) or CAF diet before and during pregnancy and lactation. Female and male offspring were sacrificed after weaning at different stages of reproductive maturation—females on postnatal days (PNDs) 30, 35, and 60, and males on PNDs 40 and 60. Ovaries and testis were examined for the expression of the kisspeptin system, including <i>Kiss1</i>, <i>Kiss1r</i>, estrogen (<i>Esr1</i>, <i>Esr2</i>), androgen (<i>Ar</i>), and luteinizing hormone choriogonadotropin (Lhcgr) receptors. Additionally, morphological parameters of the ovaries and testes were evaluated.</p> Results <p>Male offspring of CAF mothers showed: i) alterations in <i>Ar</i> and <i>Kiss1</i> mRNA levels, and ii) decreased seminiferous tubules diameter and epithelium height, a reduced number of Sertoli cells, a lower percentage of seminiferous tubules with presented spermatozoa. Female offspring of CAF mothers exhibited: i) disturbed expression of <i>Esr1</i>, <i>Esr2</i>, <i>Ar</i>, and <i>Lhcgr</i> receptors in the ovaries, and ii) a diminished number of primordial and secondary follicles at PND 30 and primary follicles at PND 35.</p> Conclusions <p>We concluded that the maternal CAF diet leads to sex-specific alterations in the reproductive parameters of offspring.</p> Graphical Abstract <p></p>