CONSEQUENCES OF OBESITY AND CHEMOTHERAPY ON THE GUSTATORY SYSTEM
| dc.contributor.author | Harnischfeger, Fiona | |
| dc.contributor.chair | Dando, Robin | |
| dc.contributor.committeeMember | Tumbar, Tudorita | |
| dc.contributor.committeeMember | Just, David R. | |
| dc.date.accessioned | 2021-03-12T17:38:14Z | |
| dc.date.available | 2021-03-12T17:38:14Z | |
| dc.date.issued | 2020-08 | |
| dc.description | 144 pages | |
| dc.description.abstract | The taste system acts as a gatekeeping mechanism, to protect from toxins, and allows humans to select foods that contain beneficial nutrients. In developed countries, undernutrition arising from food availability problems has largely been addressed, whereas overnutrition leading to obesity has become an increasingly pressing issue. The gustatory system has long been neglected as a target to regulate food intake, to address overconsumption. Taste serves in guiding dietary selection, thus any change in taste in the obese, would offer an explanation for the altered behaviors around food in the obese. In the following chapters we will focus on further understanding obesity and diet induced changes to the taste bud. First, we will discuss the link between obesity-induced taste dysfunction and food intake with a focus on the appetitive tastes. Then, building on previous research, we will show that diet induced obesity, independent of calorie source, causes loss of taste buds in Sprague Dawley rats. A loss of taste buds with obesity has previously been reported in mice and humans, with both showing correlations between fungiform papillae density and weight. Additionally, in rat circumvallate papillae, taste buds are negatively correlated with caspase-positive cells, a marker for apoptosis, implying that taste buds are being actively broken down in obesity. Next, we show that dieting C57BL/6 mice to a lean weight, after previously being obese, allows mice to partially, but not fully recover taste buds. Concurrently we show reduced proliferative capacity, an increase in apoptosis and an elevation in the harmful cytokine TNF_ in both female and male mice with obesity, effects partially rescued by dieting mice. Understanding the underlying mechanisms driving obesity related taste changes will give a better understanding of the scope for future intervention strategies. Finally, we will examine changes to the taste bud after chemotherapeutic treatment, where taste deficiencies are commonly reported, and in which dietary intake is again of great importance to determining health outcomes. | |
| dc.identifier.doi | https://doi.org/10.7298/phgs-tz66 | |
| dc.identifier.other | Harnischfeger_cornellgrad_0058F_12206 | |
| dc.identifier.other | http://dissertations.umi.com/cornellgrad:12206 | |
| dc.identifier.uri | https://hdl.handle.net/1813/102877 | |
| dc.language.iso | en | |
| dc.subject | Diet | |
| dc.subject | Inflammation | |
| dc.subject | Metabolism | |
| dc.subject | Obesity | |
| dc.subject | Satiety | |
| dc.subject | Taste | |
| dc.title | CONSEQUENCES OF OBESITY AND CHEMOTHERAPY ON THE GUSTATORY SYSTEM | |
| dc.type | dissertation or thesis | |
| dcterms.license | https://hdl.handle.net/1813/59810 | |
| thesis.degree.discipline | Food Science and Technology | |
| thesis.degree.grantor | Cornell University | |
| thesis.degree.level | Doctor of Philosophy | |
| thesis.degree.name | Ph. D., Food Science and Technology |
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