Leptin is a hormone produced by adipose tissue that regulates energy balance by controlling appetite and metabolism. It inhibits orexigenic AGRP neurons and activates anorexigenic POMC neurons. However, while AGRP neurons rapidly regulate food intake, POMC neurons have a minimal effect on acute food intake. This suggests the existence of an unidentified leptin-regulated neural population that rapidly suppresses appetite. The study identifies a new population of leptin-target neurons in the arcuate nucleus expressing Bnc2, which acutely suppress appetite by directly inhibiting AGRP neurons. These neurons are modulated by leptin, sensory food cues, and nutritional status. Deleting leptin receptors in BNC2 neurons caused hyperphagia and obesity, similar to that observed in AGRP neurons. BNC2 neurons are a key component of the neural circuit that maintains energy balance. They are activated by leptin or food presence and are inhibited by AGRP neurons. BNC2 neurons also regulate glucose metabolism and insulin sensitivity. The study shows that BNC2 neurons are a new population of leptin-responsive neurons that play a critical role in regulating food intake and energy balance. The findings add an important new component to the neural circuit that regulates appetite and adiposity, while also shedding new light on the mechanisms by which leptin regulates this system.Leptin is a hormone produced by adipose tissue that regulates energy balance by controlling appetite and metabolism. It inhibits orexigenic AGRP neurons and activates anorexigenic POMC neurons. However, while AGRP neurons rapidly regulate food intake, POMC neurons have a minimal effect on acute food intake. This suggests the existence of an unidentified leptin-regulated neural population that rapidly suppresses appetite. The study identifies a new population of leptin-target neurons in the arcuate nucleus expressing Bnc2, which acutely suppress appetite by directly inhibiting AGRP neurons. These neurons are modulated by leptin, sensory food cues, and nutritional status. Deleting leptin receptors in BNC2 neurons caused hyperphagia and obesity, similar to that observed in AGRP neurons. BNC2 neurons are a key component of the neural circuit that maintains energy balance. They are activated by leptin or food presence and are inhibited by AGRP neurons. BNC2 neurons also regulate glucose metabolism and insulin sensitivity. The study shows that BNC2 neurons are a new population of leptin-responsive neurons that play a critical role in regulating food intake and energy balance. The findings add an important new component to the neural circuit that regulates appetite and adiposity, while also shedding new light on the mechanisms by which leptin regulates this system.