Obesity, a widespread health issue, accompanied by various metabolism-related disabilities, has emerged as a significant public health challenge. Primary intervention for obesity involves lifestyle changes, including dietary treatments. The ketogenic diet (KD) is increasingly recognized as a potential remedy for obesity, with its efficacy attributed to appetite suppression in the hypothalamus.The study aimed to evaluate how the metabolic changes in hypothalamus, associated with obesity affect the mechanisms responsible for appetite regulation during KD treatment.Adult male mice were subjected to Western-style diet for 6 weeks to induce obesity (DIO), while the control mice were fed with standard chow (CTL). Then, DIO and CTL mice received a KD (DIO-KD, CTL-KD) or standard chow (DIO-SD, CTL-SD) and the body weight was evaluated after 2 weeks. Nutritional behavior was assessed using the palatable meal test and food-risk competition test. At the end of the experiment serum and hypothalamus samples were collected.Behavioral evaluation showed that the KD suppresses appetite in DIO and CTL mice. Caloric intake remained consistent during weight loss, regardless of diet. Obesity affects the serum concentration of ghrelin and leptin. The KD in obese and lean mice changed the expression levels of Agrp, Mc3r, Cart, while the DIO affected Mc4r expression in SD fed mice. An increase in Pomc expression was noted in the DIO-KD group compared to the CTL-SD group.In conclusion, KD changes nutrition behavior, which may be associated with regulation of hypothalamic expression of appetite-related genes in adult obese and lean mice.