This is further strengthened by a recent study of a hypothalamic Lphn1 knockout mouse model where female mice are protected from obesity.58 Our analysis reveals that Lphn1 knockout mice exhibit higher carbohydrate oxidation compared to fat oxidation (Fig. 2), in contrast to db/db mice, which carry a mutation in the leptin receptor and demonstrate the opposite metabolic pattern.62 Generally, it was anticipated that mice would metabolize more fatty acids than carbohydrates due to the presence of accumulated fat. The gene discussed is LEPR; the disease is obesity disorder.