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.

Highlights

  • Worldwide, the prevalence of obesity, which is defined by having a body mass index (BMI) of 30 kg/m2 or higher nearly tripled since 1975 [1]

  • To further elucidate the biological and neural underpinnings of obesity, we investigated the association between brain-derived neurotrophic factor (BDNF) levels and brain response to food stimuli and craving in patients suffering from obesity and normal-weight participants by conducting a prospective case–control fMRI study

  • It might not be intuitive that peripheral BDNF levels are associated with brain response to visual cues, it has been shown that the CREB-BDNF pathway was significantly associated with activation in the precuneus, superior parietal lobule, and posterior cingulate in drinkers suffering from severe alcohol addiction [29]

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Summary

Introduction

The prevalence of obesity, which is defined by having a body mass index (BMI) of 30 kg/m2 or higher nearly tripled since 1975 [1]. In 2016, more than 1.9 billion adults were overweight or obese [1]. This is clinically relevant since obesity is associated with a significant increase in all-cause mortality [2]. Obesity is a major risk factor for type 2 diabetes mellitus, cardiovascular disease, hypertension and influences on the development of osteoarthritis and some forms of cancer, including breast, prostate, liver and colon [3]. The treatment of obesity is limited by insufficient efficacy and high risk for regaining of weight [3]. The unsatisfactory treatment effects are partly because the current knowledge of the pathophysiology of obesity, and especially on factors that modulate appetitive mechanisms remains elusive

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