Sensing Via Intestinal Sweet Taste Pathways

Richard L Young

doi:10.3389/fnins.2011.00023

Abstract

The detection of nutrients in the gastrointestinal (GI) tract is of fundamental significance to the control of motility, glycemia and energy intake, and yet we barely know the most fundamental aspects of this process. This is in stark contrast to the mechanisms underlying the detection of lingual taste, which have been increasingly well characterized in recent years, and which provide an excellent starting point for characterizing nutrient detection in the intestine. This review focuses on the form and function of sweet taste transduction mechanisms identified in the intestinal tract; it does not focus on sensors for fatty acids or proteins. It examines the intestinal cell types equipped with sweet taste transduction molecules in animals and humans, their location, and potential signals that transduce the presence of nutrients to neural pathways involved in reflex control of GI motility.

Highlights

The ability to sense the chemical composition of ingested material and respond appropriately is critical to individual survival
Studies revealed that disruption of vagal pathways via subdiaphragmatic vagotomy or afferent denervation largely or completely blocked inhibition of Abbreviations: 5-HT, 5-hydroxytryptamine; ATP, adenosine 5′-triphosphate; cAMP, 3′-5′-cyclic adenosine monophosphate; CCK, cholecystokinin; EC, enterochromaffin cells; GABA, γ-aminobutyric acid; GI, gastrointestinal; glucose-dependent insulinotropic peptide (GIP), gastric inhibitory polypeptide; GLP-1, glucagon-like peptide-1; GLP-2, glucagon-like peptide-2; G-protein coupled receptors (GPCR), G-protein coupled receptor; IP3, inositol trisphosphate; PLCβ2, phospholipase Cβ2; PYY, peptide YY; T1Rx, type 1 taste receptor family (T1R2 + T1R3 = sweet, T1R1 + T1R3 = umami); T2R, type 2 taste receptor family; TRPM4, type-4 melastatin transient receptor potential cation channel; TRPM5, type-5 melastatin transient receptor potential cation channel
Our work extended this key finding to reveal that immunolabeling for α-gustducin was expressed throughout the GI tract with peak expression in epithelial cells of the mid-jejunum (Sutherland et al, 2007a), where carbohydrateinduced reflexes are likely to be initiated (Lin et al, 1989)

Summary

Sensing via intestinal sweet taste pathways

Discipline of Medicine, School of Medicine, University of Adelaide, Adelaide, SA, Australia. The detection of nutrients in the gastrointestinal (GI) tract is of fundamental significance to the control of motility, glycemia and energy intake, and yet we barely know the most fundamental aspects of this process This is in stark contrast to the mechanisms underlying the detection of lingual taste, which have been increasingly well characterized in recent years, and which provide an excellent starting point for characterizing nutrient detection in the intestine. This review focuses on the form and function of sweet taste transduction mechanisms identified in the intestinal tract; it does not focus on sensors for fatty acids or proteins. It examines the intestinal cell types equipped with sweet taste transduction molecules in animals and humans, their location, and potential signals that transduce the presence of nutrients to neural pathways involved in reflex control of GI motility

Introduction

Intestinal sweet taste transduction

None known

Other mechanisms of peripheral glucose detection

Findings

Conclusion