BDNF influences neural cue-reactivity to food stimuli and food craving in obesity

Abstract

There is increasing evidence that brain-derived neurotrophic factor (BDNF) impacts on the development of obesity. We are the first to test the hypothesis that BDNF levels might be associated with neural reactivity to food cues in patients suffering from obesity and healthy controls. We assessed visual food cue-induced neural response in 19 obese patients and 20 matched controls using functional magnetic resonance imaging and analyzed the associations between BDNF levels, food cue-reactivity and food craving. Whole-brain analysis in both groups revealed that food cues elicited higher neural activation in clusters of mesolimbic brain areas including the insula (food > neutral). Patients suffering from obesity showed a significant positive correlation between plasma BDNF levels and visual food cue-reactivity in the bilateral insulae. In addition, patients suffering from obesity with positive food cue-induced insula activation also reported significantly higher food craving than those with low cue-reactivity—an effect that was absent in normal weight participants. The present findings implicate that BDNF levels in patients suffering from obesity might be involved in food craving and obesity in humans. This highlights the importance to consider BDNF pathways when investigating obesity and obesity treatment.

(Epi)genetic Aspects of Metabolic Syndrome Pathogenesis in Relation to Brain-derived Neurotrophic Factor Expression: A Review

“…In addition, a low BDNF concentration in the peripheral blood of obese patients was associated with a visual response to a food signal, resulting in increased food craving. 57 Moreover, amniocentesis revealed a negative correlation between the maternal prepregnancy BMI and the BDNF concentration, confirming the effect of BDNF at the fetoplacental interface (Fig. 1).…”

The Role of Adipokines and Myokines in the Pathogenesis of Different Obesity Phenotypes—New Perspectives

“…Patients with obesity reported a significant positive correlation between visual food cue-reactivity and plasma BDNF levels. The same study, however, did not observe different BDNF levels or differences in food cravings in obese participants compared to normal-weight participants [142]. It can be inferred that a defective BDNF molecule or a defective TrkB receptor contributes to obesity through impaired control of food intake but does not directly result in stimulation of AT formation [143,144].…”

Neuroanatomical profile of BMI implicates impulsive delay discounting and general cognitive ability

“…Additionally, the regions of the SN have been linked to drug craving [35] and inhibitory control of behavior [36]. These regions have been found to exhibit neural activation in response to visual food stimuli [37] and to have abnormal functional connectivity with regions involved with reward and somatosensory processing during visual and auditory presentation of high‐calorie food cues [38]. We also found the entorhinal cortex, as a hub of the medial temporal DMN subsystem [39], to be a key part of the neuroanatomical profile of BMI.…”