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Olfactory sensory neuron-specific IGF1R knockout in mice results in increased smell perception, insulin resistance and adiposity

ABSTRACT: Olfaction is fundamental for survival but there is little known about the connection between smell perception and metabolism. In this study we implemented IGF1R knockout mice in the olfactory sensory neurons, by olfactory marker protetin (OMP) Cre specific recombination, and investigated metabolic parameters, smell perception and transcriptome sequencing. We could demonstrate that IGF1R knockout in the olfactory sensory neurons results in enhanced smell perception, insulin resistance under normal chow diet conditions and increased adiposity in mice fed control diet. Transcriptome analysis of the olfactory epithelium revealed differential expression of markers for mature and immature olfactory sensory neurons, being down-regulated and up- regulated respectively, pointing to differentiation-dependent changes that result in increased olfactory perception. Collectively, this study provides evidence that enhanced smell perception can result in insulin resistance and increased adiposity.

ORGANISM(S): Mus musculus

PROVIDER: GSE85329 | GEO | 2017/05/22

SECONDARY ACCESSION(S): PRJNA338177

REPOSITORIES: GEO

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Mus musculus

Project description:Olfactory sensory neuron-specific IGF1R knockout in mice results in increased smell perception, insulin resistance and adiposity

| PRJNA338177 | ENA

Transcription profiling of mouse olfactory sensory neurons

Project description:The overall aim of the experiment is to understand the phenotype of mature mouse olfactory sensory neurons by analyzing the transcripts expressed and enriched in them as compared to the rest of the cell types in the olfactory epithelium (consisting of immature neurons, supporting cells, progenitor cells and cells in lamina propria) and brain ( with out the olfactory bulbs). Comparision with the other cell types in the olfactory epithelium should eliminate the transcripts commonly expressed in the olfactory epithelium and comparision with brain will eliminate the transcripts common to most neurons. Our gene chip data indicates that mature mouse olfactory sensory neurons express 10,000 genes. Mature OSNs specifically contained three clusters of over represented Gene ontology categories: smell, ion transport and cilia. Analysis for the functionally over represented categories among the transcripts with a positive signal in the mature OSNs yielded largely broad categories common to all cells with the exception of chromatin modelling and RNA processing categories. Biological process categories of movement, development and immune response came as under represented categories. Experiment Overall Design: To purify mature olfactory neurons we took advantage of the OMP-GFP mice. OMP(olfactory marker protein) is expressed specifically in mature olfactory and vomeronasal sensory neurons. In the OMP-GFP mice the coding region of OMP is replaced by GFP. We purified OSNs from the rest of the epithelium from these mice by using FACS. . We used the Affymetrix gene chips mouse expression set 430 (consisting of 430A and 430B chips). Our gene chip data is extensively validated by insitu hybridizations.

2008-06-13 | E-GEOD-4915 | biostudies-arrayexpress

Persistent post-COVID-19 smell loss is associated with inflammatory infiltration and altered olfactory epithelial gene expression

Project description:We show that humans with lasting PASC olfactory loss harbor cellular and molecular changes in the olfactory epithelium, the peripheral organ for smell. Biopsy analyses using single cell RNA-sequencing, obtained from 6 patients 4-16 months following infection, identified a dysruption of olfactory epithelium homeostasis with infiltration of unique immune cell populations.

2022-12-21 | GSE201620 | GEO

Visualizing in deceased COVID-19 patients how SARS-CoV-2 attacks the respiratory and olfactory mucosae but spares the olfactory bulb

Project description:Anosmia, the loss of smell, is a common and often the sole symptom of COVID-19. The onset of the sequence of pathobiological events leading to olfactory dysfunction remains obscure. Here, we have developed a postmortem bedside surgical procedure to harvest endoscopically samples of respiratory and olfactory mucosae and whole olfactory bulbs. Our cohort of 85 cases included COVID-19 patients who died a few days after infection with SARS-CoV-2, enabling us to catch the virus while it was still replicating. We found that sustentacular cells are the major target cell type in the olfactory mucosa. We failed to find evidence for infection of olfactory sensory neurons, and the parenchyma of the olfactory bulb is spared as well. Thus, SARS-CoV-2 does not appear to be a neurotropic virus. We postulate that transient insufficient support from sustentacular cells triggers transient olfactory dysfunction in COVID-19. Olfactory sensory neurons would become affected without getting infected.

2021-10-24 | GSE176080 | GEO

Transcripts enriched in mouse olfactory sensory neurons

2007-04-30 | GSE4915 | GEO

Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation (scRNA-Seq)

Project description:A reduced sense of smell has been reported in people with cystic fibrosis (CF). These olfactory defects have largely been attributed to secondary manifestations of the disease, such as inflammation of the nasal mucosa. Here we show that CFTR, the gene responsible for CF, is expressed in proliferating olfactory human cells and that newborn CFTR null pigs display ultrastructural abnormalities in the olfactory epithelium and olfactory bulbs. In the absence of CFTR, olfactory sensory neurons still produce odor-evoked activity, but mutant animals display defective odor-guided suckling behavior after birth. Consistent with epithelial changes, we found a reduced expression of genes implicated in cell cycle and development in globose basal cells (GBCs), the neurogenic progenitor cells in the olfactory epithelium. Targeted sequencing revealed enhanced CFTR expression in the subpopulation of GBCs that is actively proliferating. Furthermore, CFTR loss caused a global reduction in the number of sensory neurons and altered olfactory receptors expression. Our findings highlight a previously unknown role of CFTR in olfactory system function by regulating progenitor cell proliferation in the olfactory epithelium.

2022-12-31 | GSE197189 | GEO

Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation (Bulk RNA-Seq)

2022-12-31 | GSE197184 | GEO

Short-term consumption of ultra-processed diets impairs the sense of smell and brain physiology [WOM]

Project description:Considering the present scenario of fast-paced life, the major shifts in eating culture in the last five decades, and the crucial role of smell in food intake, it is thus crucial to map and better understand the effects of ultra-processed diets - especially under short-term regimens - on our brain metabolism and sense of smell. To address this question, we used mice to investigate the effects of the short-term consumption of three diets varying in macronutrient composition and origin (one whole-grain-based and two ultra-processed synthetic diets) on the transcriptional profiles of the olfactory mucosa and different brain regions.

2023-11-27 | GSE217836 | GEO

Short-term consumption of ultra-processed diets impairs the sense of smell and brain physiology [Brain]

2023-11-27 | GSE217835 | GEO

single olfactory sensory neurons

Project description:single olfactory sensory neurons

| PRJEB7425 | ENA