Abstract

Type 2 Diabetes (T2D), a major public health issue reaching worldwide epidemic, has been correlated with lower olfactory abilities in humans. As olfaction represents a major component of feeding behavior, its alteration may have drastic consequences on feeding behaviors that may in turn aggravates T2D. In order to decipher the impact of T2D on the olfactory epithelium, we fed mice with a high fructose diet (HFruD) inducing early diabetic state in 4 to 8 weeks. After only 4 weeks of this diet, mice exhibited a dramatic decrease in olfactory behavioral capacities. Consistently, this decline in olfactory behavior was correlated to decreased electrophysiological responses of olfactory neurons recorded as a population and individually. Our results demonstrate that, in rodents, olfaction is modified by HFruD-induced diabetes. Functional, anatomical and behavioral changes occurred in the olfactory system at a very early stage of the disease.

Highlights

  • Mice are unable to discriminate between 2 odorants and are slower to find food in a test based on olfactory cues

  • We report that a High Fructose Diet rapidly induces early diabetic state in mice and modifies the peripheral olfactory system

  • HFruD disrupts the peripheral responses to odorants: we observe reduced amplitude and kinetics of the EOG associated with reduced sensitivity and transduction pathway capabilities in individual Olfactory sensory neurons (OSNs)

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Summary

Introduction

Mice are unable to discriminate between 2 odorants and are slower to find food in a test based on olfactory cues. After 4 weeks of diet, EOG amplitudes in response to octanol decreased in HFruD animals (p = 0.06, Supplementary Fig. 2a2) only for the highest concentration. EOG amplitudes were decreased in HFruD animals (p < 0.01, Supplementary Fig. 2b2) for all concentrations except 1:10,000.

Results
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