Thus, the observation that nesfatin-1 decreases behavioral aspects of food intake by acting within the midbrain dopamine system is of great interest as nesfatin-1 injected centrally or peripherally was shown to decrease food intake in animal models of obesity [56–58], indicating that the response to nesfatin-1 is preserved even in the state of leptin resistance. Here, NUCB2 is linked to obesity due to melanocortin 4 receptor deficiency.