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Eygret, L.

Publications and source records attributed to Eygret, L..

2 recordsLinked to original sources

Western diet reversibly alters the olfactory mucosa and impairs the response to appetitive food cues

Current feeding behaviors contribute to the epidemic levels of obesity and diabetes observed in Europe and worldwide. Together with other sensory modalities, olfaction is involved in the control of food intake. Olfactory cues can influence eating behaviors, yet the nutritional status and diet can also alter olfactory abilities. Patients with metabolic disorders present impaired olfactory sensitivity which could in turn worsen their eating behaviors. Here we examined the short-term impact of a Western diet enriched in fat and sugar (High-Fat High-Sugar, HFHS) on the anatomy and physiology of the olfactory epithelium of mice. After 8 weeks of diet, HFHS fed animals presented higher adiposity without overweight, were glucose intolerant without any change in basal blood glucose or plasma insulin. A buried food test indicated impaired olfactory capacities in the HFHS group. Whereas food related odours increased food intake in control chow fed animals, HFHS mice showed an altered response to olfactory appetitive food cues. HFHS fed mice presented olfactory sensory neurons (OSN) with shorter cilia. Finally, electro-olfactogram (EOG) recorded in response to different odorant molecules showed lower amplitudes in HFHS fed mice. HFHS diet withdrawal during one month at the end of the HFHS diet exposure improved metabolic parameters and restored both the OSN cilia length and EOGs. Our results show that diet enriched in fat and sugar can rapidly alter the physiology of the olfactory epithelium before the development of significant metabolic disorders. Anatomical changes of individual olfactory sensory neurons may participate to the reduced olfactory sensitivity.

neuroscience↗

A neuronal circuit driven by GLP-1 in the olfactory bulb regulates insulin secretion

Glucagon-like peptide 1 (GLP-1) stimulates insulin secretion and holds significant pharmacological potential. Nevertheless, the regulation of energy homeostasis by centrally-produced GLP-1 remains partially understood. Preproglucagon cells, known to release GLP-1, are found in the olfactory bulb (OB). We demonstrate that activating GLP-1 receptors (GLP-1R) in the OB stimulates insulin secretion in response to oral glucose in lean and diet-induced obese mice. This is associated with reduced noradrenaline content in the pancreas and blocked by an 2-adrenergic receptor agonist, highlighting the functional implication of the sympathetic nervous system (SNS). Inhibiting GABAA receptors in the paraventricular nucleus of the hypothalamus (PVN), the control centre of the SNS, abolishes the enhancing effect on insulin secretion induced by OB GLP-1R. Therefore, OB GLP-1-dependent regulation of insulin secretion relies on a relay within the PVN. These findings identify a novel top-down neural mechanism engaged by OB GLP-1 signaling to control insulin secretion via the SNS.

physiology↗