Attenuating saturated-fat induced changes in dopamine neurotransmission

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

Abstract: Diet-induced obesity (DIO) is associated with chronic, low-grade inflammation and correlates with mood and psychological disorders (i.e., depression and anxiety). Recent studies suggest inflammation plays a role in neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease. Dopamine acts as a key link between obesity and these other neurological conditions. Research models, timing, and the composition of the obesity-inducing diet contribute to disrupted dopamine signaling. The exact mechanism behind this interruption remains unclear but one theory is the release of pro-inflammatory cytokines from adipose tissue promotes low- grade inflammation. Saturated fats, a major component of DIO, exacerbate the inflammatory response by activating the same innate immune system receptor (toll-like receptor 4, TLR4) on macrophages and microglia. This project investigated three different approaches to reduce inflammation (diet, exercise, and pharmacology) to observe how they affect dopamine signaling (release and reuptake rate) under pro- or anti- inflammatory conditions. Our findings show that a diet high in fat (60% kcals) decreases phasic dopamine release (5p20Hz) and Vmax. Prophylacytic NSAID treatment with Ketofen counteracts these effects. However, neither dietary changes or exercise has a significant impact. Interestingly, females seem to have some protection from further inflammation when they exercise while consuming a high-fat diet. Overall, this data offers promising avenues for exploring alternative treatments for DIO.

Additional Information

Publication
Language: English
Date: 2024
Keywords
Dopamine, HFD, Inflammation, Obesity, Saturated fat

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