The current epidemic of obesity is driven, at least in part, by excessive caloric intake and fat intake has been implicated as a major contributing factor. The mammalian taste system displays marked plasticity, and it has been shown that the detection of fatty acids, the prototypical fat taste stimulus, leads to reduced sensitivity upon prolonged exposure to a high-fat diet. Increased obesity and metabolic disorders in postmenopausal females indicate that the female steroid hormone, estrogen, may contribute to metabolic homeostasis. Sex differences in the taste system were explored using a multidisciplinary approach to examine the ways in which estrogen influences the detection and recognition of fatty acids in the taste system. The findings suggest that estrogen in females is an essential factor in mediating sex differences in fat taste. Moreover, the stimulatory effect of fatty acid taste cell activation is further enhanced by estradiol (E2), suggesting a specific role of E2 in modulating peripheral fat detection. Genes and protein function important for the transduction pathway of fatty acids vary between males and females and these differences exist across the various taste papillae. In vivo support for the effect of estrogens in taste cells was provided by comparing the fatty acid responsiveness in males, intact females, and ovariectomized (OVX) female mice with and without hormone replacement. In general, females detected fatty acids at lower concentrations and the presence of circulating estrogens increased this apparent fat taste sensitivity. To study the long-term effects of fat intake in males and females, a diet-induced obesity model was used. Estrogen loss in females lead to increases in food intake, body weight, adiposity, and fat mass, and ultimately reduced taste cell activity. These metabolic effects were reversed by estrogen replacement in females. Taken together, these data indicate that increased circulating estrogens in the taste system may play a significant role in physiology and chemosensory cellular activation and, in turn, may alter taste driven behavior and overall nutrient intake.


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Graduation Date





Gilbertson, Timothy


Doctor of Philosophy (Ph.D.)


College of Medicine


Burnett School of Biomedical Sciences

Degree Program

Biomedical Sciences




CFE0008920; DP0026199





Release Date


Length of Campus-only Access

1 year

Access Status

Doctoral Dissertation (Open Access)


College of Medicine