scholarly journals Molecular evolution of umami/sweet taste receptor genes in reptiles

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5570
Author(s):  
Ping Feng ◽  
Shichu Liang
Keyword(s):  
Feeding Ecology ◽  
Feeding Habits ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Genome Database ◽  
Sweet Taste Receptor ◽  
Dietary Preferences ◽  
Representative Species ◽  
Genome Information ◽  
The Relationship

Sensory systems play an important role in animal survival. Changes to these systems may be critical in evolution of species in new environments. Previous studies exploring the correlation between feeding ecology and Tas1r evolution mainly focused on mammals and birds, and found that the relationship was complex. However, in reptiles, the correlation between Tas1r evolution and dietary preferences is still unclear. Here, we attempted to explore this relationship in representative species of the major groups of reptiles (turtles, snakes, lizards, crocodilians), for which the genome information is known. We first predicted the functionality (intact, partial, or defective) of Tas1r, and then related it to the feeding preferences. As a result, we identified 11 Tas1r1, 12 Tas1r2, and 12 Tas1r3 genes to be partial or intact and another 22 Tas1r genes to be absent or pseudogenized in the 19 reptiles. We found that, as it was revealed in some other vertebrate groups, no correlation existed between feeding ecology and Tas1r evolution in reptiles: genomic prediction indicated that the Tas1r genes possibly have been lost or pseudogenized in snakes, but in crocodylia and testudines Tas1r genes are either intact or partial, regardless of their feeding habits. Thus, we suggest that the driving force of Tas1r evolution in reptiles is complex, and the feeding habit of swallowing food whole without chewing or the absence of taste buds in certain species may account for the possible umami/sweet perception loss. In addition, we propose that caution should be taken when predicting gene functionality from the publicly available genome database.

scholarly journals New Insights on the Evolution of the Sweet Taste Receptor of Primates Adapted to Harsh Environments

Animals ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 2359
Author(s):  
Nur Aida Md Tamrin ◽  
Ramlah Zainudin ◽  
Yuzine Esa ◽  
Halimah Alias ◽  
Mohd Noor Mat Isa ◽  
...  
Keyword(s):  
Phylogenetic Trees ◽  
Environmental Changes ◽  
Receptor Gene ◽  
Taste Receptor ◽  
Sensory Information ◽  
Sweet Taste ◽  
Taste Perception ◽  
Sweet Taste Receptor ◽  
Dietary Preferences ◽  
Starting Point

Taste perception is an essential function that provides valuable dietary and sensory information, which is crucial for the survival of animals. Studies into the evolution of the sweet taste receptor gene (TAS1R2) are scarce, especially for Bornean endemic primates such as Nasalis larvatus (proboscis monkey), Pongo pygmaeus (Bornean orangutan), and Hylobates muelleri (Muller’s Bornean gibbon). Primates are the perfect taxa to study as they are diverse dietary feeders, comprising specialist folivores, frugivores, gummivores, herbivores, and omnivores. We constructed phylogenetic trees of the TAS1R2 gene for 20 species of anthropoid primates using four different methods (neighbor-joining, maximum parsimony, maximum-likelihood, and Bayesian) and also established the time divergence of the phylogeny. The phylogeny successfully separated the primates into their taxonomic groups as well as by their dietary preferences. Of note, the reviewed time of divergence estimation for the primate speciation pattern in this study was more recent than the previously published estimates. It is believed that this difference may be due to environmental changes, such as food scarcity and climate change, during the late Miocene epoch, which forced primates to change their dietary preferences. These findings provide a starting point for further investigation.

scholarly journals Nutrient sensing of gut luminal environment

2020 ◽  
pp. 1-8
Author(s):  
A. W. Moran ◽  
K. Daly ◽  
M. A. Al-Rammahi ◽  
S. P. Shirazi-Beechey
Keyword(s):  
Metabolic Diseases ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Nutrient Sensing ◽  
Sweet Taste Receptor ◽  
Nutritional Recommendations ◽  
Neuronal Signalling ◽  
The Relationship ◽  
G Protein Coupled ◽  
Diabetes And Obesity

Sensing of nutrients by chemosensory cells in the gastrointestinal tract plays a key role in transmitting food-related signals, linking information about the composition of ingested foods to digestive processes. In recent years, a number of G protein-coupled receptors (GPCR) responsive to a range of nutrients have been identified. Many are localised to intestinal enteroendocrine (chemosensory) cells, promoting hormonal and neuronal signalling locally, centrally and to the periphery. The field of gut sensory systems is relatively new and still evolving. Despite huge interest in these nutrient-sensing GPCR, both as sensors for nutritional status and targets for preventing the development of metabolic diseases, major challenges remain to be resolved. However, the gut expressed sweet taste receptor, resident in L-enteroendocrine cells and responsive to dietary sweetener additives, has already been successfully explored and utilised as a therapeutic target, treating weaning-related disorders in young animals. In addition to sensing nutrients, many GPCR are targets for drugs used in clinical practice. As such these receptors, in particular those expressed in L-cells, are currently being assessed as potential new pathways for treating diabetes and obesity. Furthermore, growing recognition of gut chemosensing of microbial-produced SCFA acids has led further attention to the association between nutrition and development of chronic disorders focusing on the relationship between nutrients, gut microbiota and health. The central importance of gut nutrient sensing in the control of gastrointestinal physiology, health promotion and gut–brain communication offers promise that further therapeutic successes and nutritional recommendations will arise from research in this area.

Interaction of suosan with the sweet taste receptor

1982 ◽  
Vol 175 (4) ◽  
pp. 266-268 ◽  
Author(s):  
Jean-Marie Tinti ◽  
Claude Nofre ◽  
Anne-Marie Peytavi
Keyword(s):  
Taste Receptor ◽  
Sweet Taste ◽  
Sweet Taste Receptor

scholarly journals Transformation of postingestive glucose responses after deletion of sweet taste receptor subunits or gastric bypass surgery

2012 ◽  
Vol 303 (4) ◽  
pp. E464-E474 ◽  
Author(s):  
Maartje C. P. Geraedts ◽  
Tatsuyuki Takahashi ◽  
Stephan Vigues ◽  
Michele L. Markwardt ◽  
Andongfac Nkobena ◽  
...  
Keyword(s):  
Gastric Bypass ◽  
Glycemic Control ◽  
Large Intestine ◽  
Molecular Mechanisms ◽  
Hormone Secretion ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Oral Glucose ◽  
Isolated Pancreatic Islets ◽  
Sweet Taste Receptor

The glucose-dependent secretion of the insulinotropic hormone glucagon-like peptide-1 (GLP-1) is a critical step in the regulation of glucose homeostasis. Two molecular mechanisms have separately been suggested as the primary mediator of intestinal glucose-stimulated GLP-1 secretion (GSGS): one is a metabotropic mechanism requiring the sweet taste receptor type 2 (T1R2) + type 3 (T1R3) while the second is a metabolic mechanism requiring ATP-sensitive K+(KATP) channels. By quantifying sugar-stimulated hormone secretion in receptor knockout mice and in rats receiving Roux-en-Y gastric bypass (RYGB), we found that both of these mechanisms contribute to GSGS; however, the mechanisms exhibit different selectivity, regulation, and localization. T1R3−/−mice showed impaired glucose and insulin homeostasis during an oral glucose challenge as well as slowed insulin granule exocytosis from isolated pancreatic islets. Glucose, fructose, and sucralose evoked GLP-1 secretion from T1R3+/+, but not T1R3−/−, ileum explants; this secretion was not mimicked by the KATPchannel blocker glibenclamide. T1R2−/−mice showed normal glycemic control and partial small intestine GSGS, suggesting that T1R3 can mediate GSGS without T1R2. Robust GSGS that was KATPchannel-dependent and glucose-specific emerged in the large intestine of T1R3−/−mice and RYGB rats in association with elevated fecal carbohydrate throughout the distal gut. Our results demonstrate that the small and large intestines utilize distinct mechanisms for GSGS and suggest novel large intestine targets that could mimic the improved glycemic control seen after RYGB.

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