Kisspeptin regulates reproduction by stimulating GnRH neurons via its receptor, Kiss1r. Kiss1r is expressed in various brain areas and peripheral tissues indicating a non-reproductive role. We recently examined the role of kisspeptin in energy balance by examining the metabolic profile of Kiss1r knockout (KO) mice, which develop an obese and diabetic phenotype. Moreover, these mice display elevated plasma leptin concentrations indicative of leptin resistance. Leptin is a hormone produced from white adipose tissue that acts as an anorexigenic signal. Interestingly, Kiss1r KO female mice exhibit reduced food intake compared to wildtype (WT) littermates, thus it is unclear whether leptin resistance is present. In addition, obesity is associated with ghrelin resistance. Ghrelin is an orexigenic hormone produced by the gut and resistance during obesity is thought to protect a higher body weight set-point established during times of food availability. Whether Kiss1r KO mice are ghrelin resistant is unknown. Therefore, we aimed to investigate whether Kiss1r KO mice responds normally to exogenous leptin or ghrelin administration. Gonadectomised male and female Kiss1r KO and WT mice (7-9 week-old) were given a single intraperitoneal injection of either saline, ghrelin (1mg/g body weight) or leptin (2mg/g body weight) (all drugs given in a volume of 100ml) at 6pm. After five hours, food intake was measured and blood and hypothalami were collected. In male and female WTs, there were non-significant trends for lower energy intake following leptin administration and ghrelin treatment resulted in a 40% increase in energy intake (P<0.05). In all Kiss1r KO mice, no changes in food intake and body weight were identified regardless of treatment group. Therefore, we can identify that Kiss1r KO mice may exhibit ghrelin resistance but leptin resistance was inconclusive. This indicates that an altered set-point in body weight regulation may be contributing to the obesity in Kiss1r KO mice.