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.
Highlights
Hedonic feelings are parts of the paramount drive in mammalian physiological systems [1]
glucagon-like peptide 1 (GLP-1) R is expressed on adjacent taste nerve fibers in the tongue
Consistent with this, we provided evidence about the role of GLP-1 in gustatory coding, mostly based on preclinical studies
Summary
Hedonic feelings are parts of the paramount drive in mammalian physiological systems [1]. Palatable foods that make us “feeling good” contain calorie-dense sweet and fat substances [2,3] In environments where such nutrients are readily available with little or no effort, we are not able to successfully resist these dietary challenges [4,5]. Obesity and diabetes are persistently accelerating [6], with almost half of United States’ (US) adults predicted to have obesity and about 34.4 million predicted to have diabetes by 2030 [7]. They both represent global public health burdens due to their epidemic occurrence and their association with adverse consequences. Considering that obesity is characterized as a condition of food intake above the physiological needs of the body, we should make further efforts in understanding how feeding behavior in obesity becomes dysfunctional and how to reverse it
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