Adiponectin Enhances the Responsiveness of the Olfactory System

Abstract

The peptide hormone adiponectin is secreted by adipose tissue and the circulating concentration is reversely correlated with body fat mass; it is considered as starvation signal. The observation that mature sensory neurons of the main olfactory epithelium express the adiponectin receptor 1 has led to the concept that adiponectin may affect the responsiveness of the olfactory system. In fact, electroolfactogram recordings from olfactory epithelium incubated with exogenous adiponectin resulted in large amplitudes upon odor stimulation. To determine whether the responsiveness of the olfactory sensory neurons was enhanced, we have monitored the odorant-induced expression of the immediate early gene Egr1. It was found that in an olfactory epithelium incubated with nasally applied adiponectin the number of Egr1 positive cells was significantly higher compared to controls, suggesting that adiponectin rendered the olfactory neurons more responsive to an odorant stimulus. To analyze whether the augmented responsiveness of sensory neurons was strong enough to elicit a higher neuronal activity in the olfactory bulb, the number of activated periglomerular cells of a distinct glomerulus was determined by monitoring the stimulus-induced expression of c-fos. The studies were performed using the transgenic mOR256-17-IRES-tauGFP mice which allowed to visualize the corresponding glomerulus and to stimulate with a known ligand. The data indicate that upon exposure to 2,3-hexanedione in adiponectin-treated mice the number of activated periglomerular neurons was significantly increased compared to controls. The results of this study indicate that adiponectin increases the responsiveness of the olfactory system, probably due to a higher responsiveness of olfactory sensory neurons.

Association between diabetes mellitus and olfactory dysfunction: current perspectives and future directions

“…The adipocytokine adiponectin appears to have a similar effect on olfactory neurons as ghrelin [57]. This observation is of particular interest, given the findings of Sanke et al [48] in elderly people with diabetes.…”

“…The ghrelin receptor (growth hormone secretagogue receptor 1a) is expressed on olfactory neurons, and exogenous intranasal ghrelin results in sensitization of olfactory neurons; however, ghrelin itself is not found in the olfactory epithelium. The adipocytokine adiponectin appears to have a similar effect on olfactory neurons as ghrelin [57]. This observation is of particular interest, given the findings of Sanke et al [48] in elderly people with diabetes.…”

Fasting induces astroglial plasticity in the olfactory bulb glomeruli of rats

“…Olfactory neural processing is closely linked to the animal's nutritional status. The activity of OB neurons is influenced by metabolic hormones, including orexins and leptin (Prud'homme et al, 2009), insulin (Aim e et al, 2012, adiponectin (Loch, Heidel, Breer, & Strotmann, 2013), and ghrelin (Loch, Breer, & Strotmann, 2015). These changes in olfaction contribute to the sensations of hunger and satiety and play a key role in triggering and terminating food intake.…”

“…A growing body of evidence suggests that metabolic factors modulate the first steps by which rodents detect odor, within the olfactory mucosa and bulb (Palouzier-Paulignan et al, 2012). The activity of OB neurons is influenced by metabolic hormones, including orexins and leptin (Prud'homme et al, 2009), insulin (Aim e et al, 2012, adiponectin (Loch, Heidel, Breer, & Strotmann, 2013), and ghrelin (Loch, Breer, & Strotmann, 2015).…”

The extremely broad odorant response profile of mouse olfactory sensory neurons expressing the odorant receptor MOR256‐17 includes trace amine‐associated receptor ligands

“…However, for the false‐positive response to cyclohexanone for MOR256‐17 and to heptanoic acid and 1‐octanethiol for SR1 [discrepancies in which a heterologous system (Saito et al ., ; Goldsmith et al ., ; Yu et al ., ) detects a response that cannot be reproduced in native OSNs that express the unmodified OR from the endogenous locus] there is no obvious explanation. The only available in vivo data for MOR256‐17 are with 2,3‐hexanedione, in a strain of MOR256‐17‐IRES‐tauGFP mice that has been generated independently (Luxenhofer et al ., ); in mice exposed to 2,3‐hexanedione, there is an increase in the percentage of c‐fos+ juxtaglomerular cells surrounding the GFP+ glomeruli (Loch et al ., ).…”