Introduction: Obesity is currently a major health problem of our modern society. Food abundance and composition are linked to the increase obesity incidence. Besides, it is now recognized that high daily consumption of sugar, fat and a lack of physical exercise contribute to obesity. Some studies have shown that the consumption of dietary fatty acids promotes sweetness perception. In this study we investigate the interaction between fat and sweet gustatory modalities.
Materials and Methods: we employed, in-vivo, behavioral approach in control and high fat diet-obese mice, using the double choice test. To investigate the interaction between fat (CD36 and GPR120) and sweet (T1R2/T1R3) receptors we performed, in-vitro, experiment on taste bud cells (TBC) such as calcium signaling, immunocytochemistry and RT-PCR
.Results: we observed that sweet taste perception was enhanced by fat (linoleic acid) and vice versa in control mice. However, fat taste perception was suppressed and sweet taste was reduced in obese mice. Interestingly, in these obese mice, the sweet taste perception was curtailed by fat component (linoleic acid). We also observed that TBC co-expressed fat receptors (CD36 and GPR120) and sweet receptors (T1R3) and sweet and fat components exerted additive calcium signaling response.
Discussion/conclusion: The reduction of fat and sweet taste sensitivity and the absence potentiation between these two gustatory modalities, in obese mice, could result from the decreases the expression of CD36-fat taste receptor (but not GPR120) and sweet receptors (T1R2/T1R3) and by the fact that GPR120 and T1R2/T1R3 shared a commune calcium-signaling pathway
Mots clés : Physiology / Nutrition/ Fat / Sweet / Taste / Obesity / Cross-Talk
Auteurs : Anthony-Damien DESIREE, Amira KHAN, Aziz HICHAMI, Naim Akhtar KHAN
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