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Review
. 2021 Jan 18;22(2):902.
doi: 10.3390/ijms22020902.

Glucagon-Like Peptide 1 and Taste Perception: From Molecular Mechanisms to Potential Clinical Implications

Mojca Jensterle  1   2 , Manfredi Rizzo  3   4 , Andrej Janez  1   2
Affiliations
Review

Glucagon-Like Peptide 1 and Taste Perception: From Molecular Mechanisms to Potential Clinical Implications

Mojca Jensterle et al. Int J Mol Sci. .

Abstract

Preclinical studies provided some important insights into the action of glucagon-like peptide 1 (GLP-1) in taste perception. This review examines the literature to uncover some molecular mechanisms and connections between GLP-1 and the gustatory coding. Local GLP-1 production in the taste bud cells, the expression of GLP-1 receptor on the adjacent nerves, a functional continuum in the perception of sweet chemicals from the gut to the tongue and an identification of GLP-1 induced signaling pathways in peripheral and central gustatory coding all strongly suggest that GLP-1 is involved in the taste perception, especially sweet. However, the impact of GLP-1 based therapies on gustatory coding in humans remains largely unaddressed. Based on the molecular background we encourage further exploration of the tongue as a new treatment target for GLP-1 receptor agonists in clinical studies. Given that pharmacological manipulation of gustatory coding may represent a new potential strategy against obesity and diabetes, the topic is of utmost clinical relevance.

Keywords: GLP-1; obesity; sweet; taste; tongue.

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Conflict of interest statement

The authors declare that the current research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. M.J. has no conflicts of interest. M.R. has given lectures, received honoraria and research support, and participated in conferences, advisory boards and clinical trials sponsored by many pharmaceutical companies including AstraZeneca, Boehringer Ingelheim, Kowa, Eli Lilly, Merck Sharp & Dohme, Novo Nordisk, Novartis, Roche Diagnostics, Sanofi and Servier; he is currently Medical Director, Novo Nordisk BA LM. A.J. has served as a consultant and is on speakers bureaus for AstraZeneca, Boehringer Ingelheim, Eli Lilly, MSD, Novo Nordisk, and Sanofi. None of the above had any role in this article, which has been written independently, without any financial or professional help, and reflects only the opinion of the authors, without any role of the industry.

Figures

Figure 1
Figure 1
Taste sensation signaling and glucagon-like peptide 1 (GLP-1). Legend: A sugar molecule binds to heterodimeric G protein coupled receptor (GPCR) that consists of taste receptor type 1 member 2 (TAS1R2) and taste receptor type 1 member 3 (TAS1R3). Downstream signaling ultimately leads to release of ATP. Specifically, upon PLCβ2 activation IP3 as a second messenger is generated. IP3 releases intracellular Ca2+. Released Ca2+ gates transient receptor potential cation channel subfamily M member 5 (TRPM5), which results in cellular depolarization. The generated action potentials cause a release of ATP through voltage-gated calcium homeostasis modulator 1 (CALMH1) that engages purinergic receptors for ATP on the sensory nerve fibers. Sensory nerve fibers convey information to higher order neurons in the Nucleus Tractus Solitarus (NTS). Adenosine triphosphate (ATP) as a transmitter represents the major line of communication from TBC type II cells to the brain. In addition, when stimulated with sweet molecules, glucagon like peptide -1 (GLP-1) is also immediately released from TBCs by vesicular mechanisms. GLP-1 activates GLP-1 receptor (GLP-1 R) on the adjacent gustatory nerves. It seems that GLP-1 acts as ancillary neurotransmitter in cooperation with ATP for maximal activation of nerve fibers that transmit gustatory code for the perception of sweet.
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