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Title page for ETD etd-06022016-170859

Type of Document Dissertation
Author Watkins, Tristan Jamison
URN etd-06022016-170859
Title Neural Correlates of Obesity: Disgust, Inflammation, and Brain Function
Degree PhD
Department Neuroscience
Advisory Committee
Advisor Name Title
Ronald L. Cowan Committee Chair
Kevin D. Niswender Committee Co-Chair
Bunmi O. Olatunji Committee Member
Christopher C. Quarles Committee Member
  • neuroinflammation
  • disgust
  • obesity
  • brain function
  • MRI
Date of Defense 2016-05-16
Availability unrestricted
Body weight is tightly controlled by the homeostatic feeding system, which is primarily reliant upon communication between the endocrine system and the brain. The endocrine system and brain are highly complex systems with multiple components that can present with altered function. Decreased neural insulin or leptin sensitivity and altered neural underpinnings of disgust are associated with obesity. As such, it is important to explore new factors that are associated with obesity and to continually expand upon existing methodologies to increase our understanding of this multi-faceted disorder.

Our results across two studies reveal the structural and functional underpinnings of Disgust Proneness, as well as how Disgust Proneness is altered in obesity. Obese individuals have lower levels of Disgust Sensitivity, as measured by the Disgust Propensity and Sensitivity Scale – Revised (DPSS-R). Using an fMRI-optimized task designed to elicit disgust and food-related disgust, we found that obese individuals have less insula BOLD activation than the lean group. This is the first identification of altered levels of BOLD activation in obese individuals within the insula. Furthermore, the self-reported measures of Disgust Sensitivity were positively correlated with insula activation extracted from the lean group, but negatively correlated with insula activation extracted from the obese group. This finding suggests that there is a functional dissociation between self-report of Disgust Sensitivity and neural activation in obese individuals. Our study did not reveal between-group differences in insula grey matter volume.

Diet- and obesity-induced parenchymal density changes have been documented in the rodent mediobasal hypothalamus using immunohistochemistry. Emerging MRI techniques are being developed to quantify these changes in parenchymal density in living humans. Our study sought to explore the viability of using single echo T1 MRI scans to identify parenchymal density changes in human subjects before and after weight loss and insulin detemir intervention. Our null results suggest that single echo T1-weighted MRI is not a suitable alternative to single or multi echo T2-weighted MRI.

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