Maternal obesity predisposes offspring to metabolic diseases. Insulin resistance and adiposity secondary to maternal calorie-rich high-fat diet consumption are considered key contributors to such developmental programming. Here, we show that non-nutritive sensory components of high-fat diet (HFD), beyond its hypercaloric, obesogenic effects, are sufficient to alter metabolic health in the offspring. To dissociate the caloric and sensory components of HFD, we fed dams a diet isonutritional to a normal chow diet but enriched with fat-related odors mimicking the sensory signature of a commonly used HFD. We show that offspring exposed to these fat-related odors during development display in adulthood increased weight gain, adiposity, and insulin resistance in response to HFD feeding independently of maternal metabolic health alterations. We employed calcium fiber photometry imaging to investigate the influence on the neuronal activity dynamics of the Agouti-related peptide (AgRP) hunger neurons. These experiments revealed that developmental exposure to fat related odors shift the AgRP neuronal responses to food cues to phenocopy those of obese mice, including desensitization to dietary fat. Collectively, we report that fat-related sensory cues during development act as instructive signals to prime central responses to food cues and whole-body metabolism regulation.