Abstract:
Emerging research increasingly suggests that triglycerides influence dopamine
pathways, impacting appetite regulation and reinforcing binge-eating behaviors. To
investigate this, we recruited 61 female participants categorized into three groups:
patients with BED, subsyndromal BED, and a control group. Each participant
completed two in-lab sessions, including diagnostic interviews, behavioral
assessments, blood draws, and reward-related tasks while undergoing MRI scans.
During the study, participants performed a FCR task, measuring BOLD response
amplitudes and functional connectivity during a food bidding task. Neural activity was
then analyzed in relation to triglyceride levels obtained from blood samples. Our
hypothesis was that elevated plasma triglyceride levels would be associated with a
reduced neural response to palatable food cues.
Through our findings, we were able to confirm this hypothesis, showing that while
individuals with BED exhibit heightened activation in reward-related brain regions,
elevated triglyceride levels correlate with a blunted response in key reward
processing areas. Subsyndromal BED participants displayed intermediate
activation, suggesting a continuum of reward sensitivity in binge eating behaviors.
Notably, higher fasting triglyceride levels were linked to reduced activation in brain
regions involved in reward processing, interoception, and memory. Significant
negative correlations between triglyceride levels and activation in the insula and
hippocampus suggest that metabolic dysregulation may dampen neural
responsiveness to food-related stimuli. Additionally, greater post-meal triglyceride
fluctuations were associated with attenuated activation in regions critical for
dopamine signaling and reward regulation. These findings suggest that chronic
overconsumption and metabolic alterations may lead to a gradual desensitization of
the brain’s reward system.
Overall, our findings highlight the critical role of metabolic factors in shaping neural
responses to food. Understanding these mechanisms could enable targeted
interventions aimed at restoring reward sensitivity and improving appetite regulation
in individuals with BED. Future research should explore how metabolic modulation
may serve as a potential therapeutic strategy for disordered eating behaviors.
Reward