The reproductive impact of persistent energy excess in the female remains incompletely defined; yet, the escalating prevalence of obesity calls for better understanding of this phenomenon. Alike, the influence of ovarian hormones on the pathophysiology of obesity and its co-morbidities merits further investigation. We study here the metabolic and gonadotropic impact of sequential obesogenic insults, namely, postnatal over-nutrition (by rearing in small litters; SL) and high fat diet (HFD) after weaning, in gonadal-intact and ovariectomized (OVX) female rats. In young (4-mo) females, SL or HFD similarly increased body weight; yet, only HFD evoked additional metabolic perturbations, some of which were worsened by precedent SL. In addition, HFD concomitantly decreased LH and estradiol levels, and, when combined with SL, suppressed Kiss1 expression in the hypothalamic arcuate nucleus (ARC) in 4-mo females, whereas HFD up to 10-mo reduced luteinizing hormone responses to kisspeptin-10 also. OVX caused rapid deterioration of the metabolic profile, with overweight, increased energy intake and deregulation of leptin and glucose/insulin levels; effects whose magnitude was similar, if not higher than HFD. Summation of previous obesogenic insults maximally increased body weight, basal leptin, insulin and glucose levels, and glucose intolerance. Yet, OVX obliterated the inhibitory effects of overweight/HFD on gonadotropin levels and ARC Kiss1 expression. Our study documents the deleterious consequences of sequential obesogenic insults on the female gonadotropin axis, which involve central impairment of Kiss1 system. In addition, our work delineates the dramatic impact of the loss of ovarian secretions, as menopausal model, on the metabolic profile of female rats, especially when combined with preceding obesogenic challenges.