To understand hindbrain pathways involved in the control of food intake, we examined roles for calcitonin receptor (CALCR)-containing neurons in the NTS. Ablation of NTS Calcr abrogated the long-term suppression of food intake, but not aversive responses, by CALCR agonists. Similarly, activating Calcr^NTS neurons decreased food intake and body weight but (unlike neighboring Cck^NTS cells) failed to promote aversion, revealing that Calcr^NTS neurons mediate a non-aversive suppression of food intake. While both Calcr^NTS and Cck^NTS neurons decreased feeding via projections to the PBN, Cck^NTS cells activated aversive CGRP^PBN cells while Calcr^NTS cells activated distinct non-CGRP PBN cells. Hence, Calcr^NTS cells suppress feeding via non-aversive, non-CGRP PBN targets. Additionally, silencing Calcr^NTS cells blunted food intake suppression by gut peptides and nutrients, increasing food intake and promoting obesity. Hence, Calcr^NTS neurons define a hindbrain system that participates in physiological energy balance and suppresses food intake without activating aversive systems.