Leptin-sensitive OBP-expressing mucous cells in rat olfactory epithelium: a novel target for olfaction-nutrition crosstalk?

Abstract

Although odorant-binding proteins (OBP) are one of the most abundant classes of proteins in the mammalian olfactory mucus, they have only recently been ascribed a functional role in the detection of odorants by olfactory neurons. Among the three OBPs described in the rat, OBP-1f is mainly secreted by the lateral nasal glands (LNG) and Bowman's glands, and its expression is transcriptionally regulated by food deprivation in the olfactory mucosa, but not in LNG. Therefore, mucus composition might be locally regulated by hormones or molecules relevant to nutritional status. Our aim has been to investigate the mechanisms of such physiological regulation at the cellular level, through both the examination of OBP-1f synthesis sites in the olfactory mucosa and their putative regulation by leptin, a locally acting satiety hormone. Immunohistochemical observations have allowed the identification of a novel population of OBP-1f-secreting cells displaying morphological and functional characteristics similar to those of epithelial mucous cells. Ultrastructural analyses by both transmission and scanning electron microscopy has enabled a more complete cytoarchitectural characterization of these specialized olfactory mucous cells in their tissue environment. These globular cells are localized in discrete zones of the olfactory epithelium, mainly in the fourth turbinate, and are often scattered from the basal to the apical surface of the epithelium. They contain numerous small droplets of mucosubstances. Using an in-vitro-derived model of olfactory mucosa primary culture, we have been able to demonstrate that leptin increases the production of mucus by these cells, so that they constitute potential targets for the physiological modulation of mucus composition by nutritional cues.

Olfactory ability and object memory in three mouse models of varying body weight, metabolic hormones, and adiposity

“…MC4R signaling is downstream of the leptin receptor expressing POMC neurons of the hypothalamus known to regulate energy balance [63]. Leptin receptors are also expressed in the olfactory epithelium [18, 21, 64] and the olfactory bulb [65], but have never been linked with MC4R signaling there. Despite reported leptin resistance in the MC4R-null mice, the high circulating peripheral leptin levels could be acting at the level of the olfactory epithelium, which is outside the blood brain barrier, or at the level of the OB which has not been tested for leptin resistance, to decrease olfactory sensitivity resulting in poor performance on the discrimination test and the slower retrieval time in the anosmia test.…”

Olfaction Under Metabolic Influences

“…A faint labeling of basal progenitor cells is also observed. Finally, a set of discrete leptinsensitive mucous cells, which secrete odorant-binding proteins involved in odorant-receptor interaction, is also evidenced in the OM (Badonnel et al 2009).…”

Metabolic and hedonic drives in the neural control of appetite: who is the boss?

“…The first indication that hormones reflecting metabolic state (caloric demand) may affect ingestive behavior (caloric intake) by modulating sensory perception was provided by the observations that leptin and insulin administration decreased gustatory and olfactory perception [5–7] [8]. Leptin may suppress sweet taste via leptin responsive lingual taste cells [5], and may modulate olfaction by changing mucous production in olfactory mucosal cells, which secrete odorant-binding proteins important in the detection of odorants by olfactory neurons [9]. …”