Diet-induced obesity impairs dopamine to alter food behaviors

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Conner Wallace (Creator)
Institution
The University of North Carolina at Greensboro (UNCG )
Web Site: http://library.uncg.edu/
Advisor
Steven Fordahl

Abstract: Obesity prevalence has been increasing for decades with food intake patterns being a strong contributor to weight gain. Food intake is controlled through multiple brain networks, and diet-induced disruption to dopamine neurochemistry could promote overeating of palatable foods high in energy density from added fats and sugars. Intake of palatable foods acutely increases dopamine neurotransmission in the dorsal striatum and ventral striatum (nucleus accumbens (NAc)), which play roles in motivation to obtain and consume food and reward-based learning. Conversely, long-term intake of a diet high in saturated fat (HFD) diminishes the capacity for dopamine release and reuptake and impairs dopamine receptor signaling, which may promote overeating to stimulate the dopamine system. However, the precise physiological mechanisms by which HFD intake diminishes dopamine neurotransmission to alter food-related behaviors are not fully characterized. Therefore, the purpose of the presented articles included exploring contributions of inflammatory and ?-opioid receptor stress systems and insulin resistance specifically upregulated by a HFD to alter dopamine neurotransmission and whether diet-linked effects could be paired to changes in behavior. Results presented herein suggest that sensitivity to proinflammatory cytokines to reduce NAc dopamine release are heightened by HFD intake, and replacement of a preferred HFD with a less palatable low-energy dense option promotes diet-related anxiety related to potentiated sensitivity of the ?-opioid receptor system to diminish dopamine tone. Further, whereas insulin in the striatum was exhibited to induce satiety and control food preference in lean controls after feeding, HFD intake induced near-total dietary inflexibility towards alternate palatable treats. Overall, HFD-induced obesity promoted insulin resistance and sensitivity to proinflammatory and ?-opioid receptor signaling that altered NAc dopamine neurotransmission linked to alterations in food-related behaviors, and these changes may promote cravings for palatable foods that inhibit weight loss attempts by obese individuals.

Additional Information

Publication
Dissertation
Language: English
Date: 2021
Keywords
Dopamine neurochemistry, High-fat diet, Inflammation, Insulin resistance, Nucleus accumbens, Obesity
Subjects
Neurochemistry
Dopamine
Obesity
Diet
Insulin resistance
Inflammation

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