Diabetes Metab J.  2020 Aug;44(4):509-528. 10.4093/dmj.2020.0058.

Consequences of Obesity on the Sense of Taste: Taste Buds as Treatment Targets?

Affiliations
  • 1Helmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG) of the Helmholtz Center Munich at the University of Leipzig and University Hospital Leipzig, Leipzig, Germany.
  • 2Medical Department III (Endocrinology, Nephrology and Rheumatology), University of Leipzig, Leipzig, Germany.

Abstract

Premature obesity-related mortality is caused by cardiovascular and pulmonary diseases, type 2 diabetes mellitus, physical disabilities, osteoarthritis, and certain types of cancer. Obesity is caused by a positive energy balance due to hyper-caloric nutrition, low physical activity, and energy expenditure. Overeating is partially driven by impaired homeostatic feedback of the peripheral energy status in obesity. However, food with its different qualities is a key driver for the reward driven hedonic feeding with tremendous consequences on calorie consumption. In addition to visual and olfactory cues, taste buds of the oral cavity process the earliest signals which affect the regulation of food intake, appetite and satiety. Therefore, taste buds may play a crucial role how food related signals are transmitted to the brain, particularly in priming the body for digestion during the cephalic phase. Indeed, obesity development is associated with a significant reduction in taste buds. Impaired taste bud sensitivity may play a causal role in the pathophysiology of obesity in children and adolescents. In addition, genetic variation in taste receptors has been linked to body weight regulation. This review discusses the importance of taste buds as contributing factors in the development of obesity and how obesity may affect the sense of taste, alterations in food preferences and eating behavior.


Keyword

Dysgeusia; Feeding behavior; Food preferences; Obesity; Taste; Taste buds; Taste perception

Figure

  • Fig. 1 Effects of obesity on the sense of taste and its relation to food intake. Food intake is driven by the interplay of hedonic and homeostatic feedback. During digestion, a variety of factors (meal quantity, nutrients, energy status, fermentation) feedback the nutrient load and energy status of the body towards the brain and control hunger and satiety circuits. However, the earliest signal priming the cephalic phase response is food quality reflected by smell and taste, which, moreover is the key driver for the reward driven hedonic eating. The earliest signals of food intake are processed in taste buds located on the tongue surface. Taste buds are very complex and consist of three functional taste cells (type I, type II, type III) and basal cells which can develop into either adult taste cell. Basal cells are post-mitotic cells which derive from proliferating progenitor cells clustering outside the taste bud and ensuring a lifelong cell turnover. Obesity is associated with alterations in taste sensation. This may be partially explained by the contribution of obesity on taste bud signaling, homeostasis and renewal. Thereby, the huge variety of factors potentially influencing the sense of taste on the level of taste buds (adipokines, cytokines, hormones etc.) may derive from the circulation, but also the salivary glands, local fat cells or even endocrine taste cells. CCK, cholecystokinin; GLP-1, glucagon like peptide 1; PYY, peptide YY.

  • Fig. 2 Schematic presentation of cell signaling within taste bud cells. Type II cells express G-protein coupled receptors (GPRs) for bitter (taste receptors type 2 [T2Rs]), sweet (taste receptor type 1 member 1 [T1R1], T1R2, T1R3) and umami (T1R1+T1R3), but also GPR40 and 120 and glycoprotein 4 (also named cluster of differentiation 36, CD36) transducing the taste quality “fatty” [15]. In addition, metabotropic glutamate receptors (mGluRs) and glucose- and sodium/glucose transporters (GLUTs, SGLT1) are thought to transduce umami and sweet, respectively [2731]. Binding of tastants to their cognate receptors increase intracellular calcium level ([Ca2+]i) which activates transient receptor potential cation channel subfamily M member 5 (TRPM5), a Ca2+/Na+ cotransporter [34]. This leads finally to an activation of the calcium homeostasis modulator protein 1 (CALHM1) which is meant to release adenosine triphosphate (ATP) [3536]. ATP signals to afferent nerve fibers via binding to P2X receptors but also feeds back in an autocrine fashion via binding to P2X and P2Y receptors on type II cells [36]. In addition, type II cells secrete Acetylcholine (Ach) which further stimulates ATP secretion [38]. Moreover, ATP activates type III cells by binding to P2Y receptors [37]. This in turn initiates the release of neurotransmitters gamma aminobutyric acid (GABA), serotonin (5-HT) and noradrenaline into the presynaptic space as consequence of raised [Ca2+]i [2540]. In addition, this release is mediated as a result of changes in pH through the uptake of H+ by ion channels such as polycystic kidney disease proteins 1 like 3 and 2 like 1 (PKD1L3, PKD2L1), inward rectifying K+ channel (KIR2.1) and the epithelial Na+ channel (ENaC) [4142434445]. GABA and 5-HT activate afferent nerve fibers but feedback to type II cells in order to decrease further ATP secretion [15]. Glutamate is released by activated nerve fibers and tune the release of GABA and 5-HT, finally shutting down ATP secretion from type II cells [15]. Type I cells seem to have glia like function as they express several ion channels (inward rectifying K+ channel [ROMK], glutamate-aspartate transporter [GLAST], ENaC) which are supposed to clear ion currents [222335]. Moreover, as ENaC has been identified in type I cells and this is thought to be the main receptor for the detection of low NaCl-salts, these cells may transduce salty [46]. Further channels involved in transducing salty are mucolipin 3 (TRPML3) and transient receptor potential cation channel subfamily V member 1 (TRPMV) [47]. However, their cellular localization has yet to be elucidated. In addition, the enzyme nucleoside triphosphate diphosphohydrolase-2 (NTPDase2) located on the surface of type I cells, is responsible for the degradation of ATP to adenosine diphosphate (ADP) [39]. In turn, sweet receptor expressing type II cells bind ADP by adenosine 2B receptors (A2B) which further increases sweet sensation [39]. TRPV1, transient receptor potential cation channel subfamily V member 1; PLCβ2, Phospholipase C beta 2.


Cited by  2 articles

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Recent Advances in Understanding Peripheral Taste Decoding I: 2010 to 2020
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