Sensory nutrition of sweet taste. Physiological, pathophysiological and pharmacological implications of T1R2/T1R3 signalling pathways on energy (glucose) and body weight homeostasis.

Taste perception plays a key role in food chose. Both taste receptors type 1 member 2 (T1R2) and member 3 (T1R3) are responsible for detecting mono- and disaccharides, and sweet taste perception is dependent of the recognition threshold (RT) of these molecules. Differences in sweet RT are mainly attributed to polymorphisms of T1R2 and T1R3 as well as their expression in taste buds, which are regulated by several hormones including glucagon, ghrelins, glucagon-like peptide, leptins and endocannabinoids. Interestingly, aging, diabetes and obesity are characterized by significant changes in sweet taste threshold, which can influence food intake and consequently contribute to the development of these pathologies. Furthermore, anti-obesity interventions such as caloric restriction, bariatric surgery and pharmacological treatments are also associated with changes in sweet taste perception. These findings suggest a relationship between the components involved in the sweet taste signalling pathways and the mechanisms underlying in the development of these pathologies. The extra-oral expression of T1Rs have been identified in different metabolically active tissues, and its involvement in glycaemic control and body weight control have been demonstrated. These findings may help to explain the afore-mentioned events. This review analyses the physiological and pathophysiological role of T1Rs in the control of energy homeostasis and body weight and the possibility of using them in the prevention of the above-mentioned high prevalence diseases, and as new therapeutic targets.