Here, we show that non-nutritive sensory components of a high-fat diet (HFD), beyond its hypercaloric, obesogenic effects, are sufficient to alter metabolic health in the offspring.
First-pass extracted concept
fat-related sensory cues
Aliases
fat-related odours, non-nutritive sensory components of a high-fat diet
Evidence Snippets
Supporting Sources
Linked Claims
Non-nutritive sensory components of a high-fat diet are sufficient to alter metabolic health in offspring.
Here, we show that non-nutritive sensory components of a high-fat diet (HFD), beyond its hypercaloric, obesogenic effects, are sufficient to alter metabolic health in the offspring.
Fat-related sensory cues during development can prime central responses to food cues and whole-body metabolism regulation.
Collectively, we report that fat-related sensory cues during development act as signals that can prime central responses to food cues and whole-body metabolism regulation.
Developmental exposure to fat-related odours shifts mesolimbic dopaminergic circuits and AgRP neuron responses to resemble those of obese mice, including desensitization of AgRP neurons to dietary fat.
Developmental exposure to fat-related odours shifts mesolimbic dopaminergic circuits and Agouti-related peptide (AgRP) hunger neurons' responses to phenocopy those of obese mice, including a desensitization of AgRP neurons to dietary fat.
Neither neonatal optogenetic activation of sensory circuits alone nor passive exposure to fat-related odours alone is sufficient to alter metabolic responses to high-fat diet.
While neither neonatal optogenetic activation of sensory circuits nor passive exposure to fat-related odours is sufficient to alter metabolic responses to HFD
Developmental exposure to fat-related odours causes offspring to display metabolic inflexibility and increased adiposity when fed a high-fat diet in adulthood independently of maternal metabolic health.
Offspring exposed to these fat-related odours during development display metabolic inflexibility and increased adiposity when fed HFD in adulthood independently of maternal metabolic health.