The olfactory bulb: A neuroendocrine spotlight on feeding and metabolism

Abstract

Olfaction is the most ancient sense and is needed for food‐seeking, danger protection, mating and survival. It is often the first sensory modality to perceive changes in the external environment, before sight, taste or sound. Odour molecules activate olfactory sensory neurons that reside on the olfactory epithelium in the nasal cavity, which transmits this odour‐specific information to the olfactory bulb (OB), where it is relayed to higher brain regions involved in olfactory perception and behaviour. Besides odour processing, recent studies suggest that the OB extends its function into the regulation of food intake and energy balance. Furthermore, numerous hormone receptors associated with appetite and metabolism are expressed within the OB, suggesting a neuroendocrine role outside the hypothalamus. Olfactory cues are important to promote food preparatory behaviours and consumption, such as enhancing appetite and salivation. In addition, altered metabolism or energy state (fasting, satiety and overnutrition) can change olfactory processing and perception. Similarly, various animal models and human pathologies indicate a strong link between olfactory impairment and metabolic dysfunction. Therefore, understanding the nature of this reciprocal relationship is critical to understand how olfactory or metabolic disorders arise. This present review elaborates on the connection between olfaction, feeding behaviour and metabolism and will shed light on the neuroendocrine role of the OB as an interface between the external and internal environments. Elucidating the specific mechanisms by which olfactory signals are integrated and translated into metabolic responses holds promise for the development of targeted therapeutic strategies and interventions aimed at modulating appetite and promoting metabolic health.

Lack of Single Amino Acids Transcriptionally Remodels Sensory Systems to Enhance the Intake of Protein and Microbiota

“…Therefore, despite significant differences in eAA functions, a deficiency in any of them can induce a similar feeding-related phenotype. These feeding decisions critically rely on chemosensory input, with taste and olfaction mediating the detection of the nutritional content of food, its toxicity, and its location [31][32][33][34] . Consequently, sensory processing has been shown to be modulated by the dietary state of the animal across phyla 32,[35][36][37][38][39][40][41][42] .…”