Eating behaviors, particularly overeating, are not only driven by nutritional requirements but also the sensory perception of food cues that predict food reward. Olfaction is often the first sensory cue of food availability and olfaction influences mood, motivation, and memory. Individuals that can’t smell show changes in the enjoyment of food and olfactory dysfunction is associated with mental and metabolic illnesses. Importantly, smell perception increases when hungry or is impaired with metabolic diseases, such as obesity. The mechanism linking metabolic state and olfaction remains unknown. Ghrelin is known as the “hunger hormone” and regulates metabolism, mood, and memory at various central nervous system (CNS) locations via its receptor under a state of energy deficit. Although the ghrelin receptors are highly expressed in the olfactory bulb (OB), their function remains unknown. We investigated whether ghrelin receptors in the OB affect olfaction and whether or not this influences mood and metabolic parameters using a viral genetic knockdown approach to chronically delete ghrelin receptors specifically in the OB in ghrelin receptor floxed mice. Deletion of ghrelin receptors in the OB significantly affected olfactory performance in olfactory discrimination and habituation tasks in both fed and fasted mice, as well as increased the latency to find food under both fasted and ghrelin-induced conditions. A two-bottle choice assay for saccharin vs water indicated that mice lacking ghrelin receptors in the OB were completely anhedonic and did not show a preference for saccharin. In support of this, we observed significantly increased anxiety and reduced exploratory locomotor activity in behavioral tasks. Intriguingly, mice increased body weight, fat mass, and blood glucose, indicating metabolic dysfunction. We conclude that OB GHSR maintains olfactory sensitivity under fasted conditions, leading to a number of behavioral and metabolic adaptations to help a mammal detect and respond appropriately to food and odor cues.