This brief report investigates the role of agouti-related protein (AgRP) neurons in regulating feeding behavior and energy homeostasis in mice. Using designer receptors exclusively activated by designer drugs (DREADD) technology, the authors demonstrate that acute activation of AgRP neurons rapidly and significantly increases food intake, reduces energy expenditure, and leads to increased fat storage. These effects are reversible upon stimulation withdrawal. Conversely, inhibiting AgRP neuronal activity in hungry mice reduces food intake. The findings suggest that AgRP neuron activity is both necessary and sufficient for feeding behavior. Additionally, activating AgRP neurons enhances motivation for feeding and drives intense food-seeking behavior, indicating their involvement in multiple levels of feeding behavior. The study highlights the utility of DREADD technology for investigating neural circuits involved in energy balance.This brief report investigates the role of agouti-related protein (AgRP) neurons in regulating feeding behavior and energy homeostasis in mice. Using designer receptors exclusively activated by designer drugs (DREADD) technology, the authors demonstrate that acute activation of AgRP neurons rapidly and significantly increases food intake, reduces energy expenditure, and leads to increased fat storage. These effects are reversible upon stimulation withdrawal. Conversely, inhibiting AgRP neuronal activity in hungry mice reduces food intake. The findings suggest that AgRP neuron activity is both necessary and sufficient for feeding behavior. Additionally, activating AgRP neurons enhances motivation for feeding and drives intense food-seeking behavior, indicating their involvement in multiple levels of feeding behavior. The study highlights the utility of DREADD technology for investigating neural circuits involved in energy balance.