Interactions between Bitter Taste, Diet and Dysbiosis: Consequences for Appetite and Obesity

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metabolic syndrome 1 endocrinologydiseases
obesity 40 endocrinologydiseases
propylthiouracil 1 endocrinologydiseasesdrugs

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propylthiouracil 7307 and disease risks.Haplotypes of TAS2R38, or phenotypes for sensitivity to the receptors ligand 6-n- propylthiouracil (PROP), are often used to define taster status. Multiple non-synonymous single nucleotide polymorphisms
Select Disease Character Offset Disease Term Instance
metabolic syndrome 14216 prevalence of obesity continues to increase worldwide and is linked to increased incidences of diabetes, metabolic syndrome , certain cancers, reduced quality of life and increased socioeconomic burdens [[42]]. It is known that
obesity 1366 receptors may be involved in modulating appetite and diet, with consequences for weight regulation and obesity . Interestingly, the concentration of T2Rs in the GI tract is greatest in the large intestine, the organ
obesity 1732 health continue to be uncovered. Of particular interest is the microbial signature associated with obesity . Obesity is a leading health concern, and advances in our understanding of this disease are needed.
obesity 1896 our understanding of this disease are needed. Diet is a known modifiable factor in the development of obesity . However, diet only partially explains disease risk. Changes in microbial energy harvesting by the microbiota
obesity 2030 partially explains disease risk. Changes in microbial energy harvesting by the microbiota plays a role in obesity , and the composition of these energy harvesting populations may be controlled by taste receptors. This
obesity 2190 populations may be controlled by taste receptors. This review explores T2Rs as a potential link between obesity and the human GI microbiome.1. IntroductionTaste is one of the five fundamental senses. It is important
obesity 4637 metabolic processes, which may alter risk for metabolic conditions including risk for diabetes and obesity [[15]]. A relationship has been established between certain microbial signatures in the GI tract and
obesity 4755 relationship has been established between certain microbial signatures in the GI tract and risk for obesity [[16]]. A decrease in the relative proportions of Bacteroidetes and a subsequent increase of Firmicutes
obesity 4918 Bacteroidetes and a subsequent increase of Firmicutes in the colon is associated with increased risk for obesity [[17],[18]]. A number of mechanisms may explain these associations, including modulations of energy
obesity 5220 genetically obese mice, compared to lean mice [[19]]. Germ-free mice are also resistant to diet-induced obesity , compared to mice with a normal gut microbiota, in a fasting-induced adipose factor dependant manner.
obesity 5644 the regulation of energy harvesting and metabolism, the GI microbiota may also contribute to risk for obesity via modulation of behaviour. Observational data suggest that gut bacteria may also play a role in the
obesity 6112 choices and GI microbiota are often analysed as individual contributing factors in the aetiology of obesity . However, obesity is a complex and multifactorial condition, and elucidating the mechanisms at play
obesity 6130 microbiota are often analysed as individual contributing factors in the aetiology of obesity. However, obesity is a complex and multifactorial condition, and elucidating the mechanisms at play requires considerations
obesity 6407 interactions between them. Furthermore, the potential role for extra-oral T2Rs in the aetiology of obesity is easily overlooked, as they are not involved in the detection of energy-containing nutrients. Therefore,
obesity 6616 Therefore, these elements are reviewed together here, with a view to creating a more complete picture of obesity in regard to bitter taste genetics, diet, and microbial compositions. These factors may interact in
obesity 8657 determinants of dietary intakes. As such, it has been hypothesised that super-tasters may be more prone to obesity , due to a reduced intake of healthy, bitter tasting, antioxidant-rich foods [[28]]. However, it appears
obesity 9470 individuals [[5],[8],[32]].A large observational study reported a significant association between risk for obesity and the TAS2R38 AVI/AVI haplotype in females [[6]]. This was also associated with increased eating disinhibition
obesity 10132 intake. Overall, high taste acuity may reduce dietary overconsumption and therefore reduce the risk for obesity , with a stronger association in females [[34]]. While TAS2R38 has been well studied, more information
obesity 10322 studied, more information is needed on the relationship between other T2R gene polymorphisms and risk for obesity . Polymorphisms in other T2R genes have been linked to other conditions, including cardiovascular disease,
obesity 11015 T1Rs (detecting energy-containing carbohydrates and amino acids) play a role in the development of obesity . However, it is becoming apparent that T2Rs are also involved in glucose regulation and the release
obesity 12481 glucose metabolism and gut motility, genetic variations in T2Rs may contribute both to the development of obesity and risk for diabetes. In addition to modulation of function via genetic variance, expression of T2Rs
obesity 14125 microbiota and GI functions such as motility [[41]]. 3. Obesity and the Gut MicrobiomeThe prevalence of obesity continues to increase worldwide and is linked to increased incidences of diabetes, metabolic syndrome,
obesity 14374 life and increased socioeconomic burdens [[42]]. It is known that diet is strongly linked to risk for obesity , and that diet also modulates the GI microbiome. This relationship was established over 100 years ago
obesity 14960 [[21]]. Over a decade ago, it was demonstrated that germ-free mice were protected against diet-induced obesity in contrast to wild-type mice with a wild-type gut microbiome [[20]]. It was shown that, when the microbiota
obesity 15450 diet [[19],[20]]. From these studies, a clear link between the composition of the gut microbiome and obesity has been established. An imbalance in the ratio of Bacteroidetes to Firmicutes phyla is more often observed
obesity 16146 species was associated with high energy intake in children [[47]]. Overall, despite individual variation, obesity displays a specific microbial signature. There is a demonstrated link between diet-induced obesity and
obesity 16245 obesity displays a specific microbial signature. There is a demonstrated link between diet-induced obesity and a bloom of Mollicutes (a class of Firmicutes). These findings suggest that dysbiosis is not only
obesity 16390 Firmicutes). These findings suggest that dysbiosis is not only caused by but can, in fact, precede obesity . It was demonstrated via mouse models that a Mollicute bloom occurred in response to diet-induced obesity
obesity 16496 obesity. It was demonstrated via mouse models that a Mollicute bloom occurred in response to diet-induced obesity and that, when this microbiome was transferred into lean germ-free mice, increased adiposity was observed
obesity 17099 fatty acids (SCFAs) as a metabolic product, and these have been implicated as aetiological factors in obesity . SCFAs are thought to stop the accumulation of fat in adipose tissue, so a decreased level is believed
obesity 17227 to stop the accumulation of fat in adipose tissue, so a decreased level is believed to contribute to obesity [[48]]. A previous study showed that animals supplemented with butyrate while on a high-fat diet displayed
obesity 17373 animals supplemented with butyrate while on a high-fat diet displayed reduced insulin resistance and obesity [[49]]. Therefore, SCFAs may offer some protection against metabolic conditions. There is a high likelihood
obesity 20136 manipulation of taste receptors. Furthermore, gastric bypass surgery, undertaken as a treatment for obesity , is known to modulate the GI microbiota [[55]]. This procedure is also known to alter taste receptor
obesity 20807 with aging [[57],[58],[59]], and it has been proposed that these changes are associated with risk for obesity through the lifespan [[60]]. Many reasons for microbiota to vary with age have already been proposed,
obesity 21322 a causative factor in changing microbial profiles. However, the direct links between taste, aging, obesity and the gastrointestinal microbiota are yet to be investigated.Some artificial sweeteners, such as saccharin
obesity 21930 to be investigated. Overall, a role for T2Rs in the complex relationship between gut microbiota and obesity may exist (Figure 4). However, further research is needed to establish this. It is important that future
obesity 22508 the interactions between taste genetics, taste receptor expression, GI microbiota, diet and risk for obesity and other diseases. It is important as we move forward to move away from the reductionist approach of
obesity 23296 each interaction may modify disease risk. T2Rs are involved in an array of mechanisms that can lead to obesity . We propose that extra-oral bitter receptors interact with gut bacteria to influence food intake and
obesity 23475 to influence food intake and gut motility, both of which influence the risk for the development of obesity . The details of such an interaction remain to be elucidated. Overall, the evidence suggests that T2Rs
obesity 23742 and a healthy microbiome. If this role can be defined, T2Rs could be manipulated to prevent or treat obesity . GPCRs are already a major drug target [[69]]. Consequently, the development of drugs to upregulate
obesity 23992 therapeutic potential. Therefore, further investigations into the role of T2Rs in the relationship between obesity and the gut microbiome are essential.Figure 1The standard paradigm linking taste genetics to risk for

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