Abstract
Excessive sucrose consumption elicits addiction-like craving that may underpin the obesity epidemic. Opioids and dopamine mediate the rewarding effects of drugs of abuse, and of natural rewards from stimuli such as palatable food. We investigated the effects of sucrose using PET imaging with [11C]carfentanil (μ-opioid receptor agonist) and [11C]raclopride (dopamine D2/3 receptor antagonist) in seven female anesthetized Göttingen minipigs. We then gave minipigs access to sucrose solution for one hour on 12 consecutive days and performed imaging again 24 hours after the final sucrose access. In a smaller sample of five minipigs, we performed an additional [11C]carfentanil PET session after the first sucrose exposure. We calculated voxel-wise binding potentials (BPND) using the cerebellum as a region of non-displaceable binding, analyzed differences with statistical non-parametric mapping, and performed a regional analysis. After 12 days of sucrose access, BPND of both tracers had declined significantly in striatum, nucleus accumbens, thalamus, amygdala, cingulate cortex and prefrontal cortex, consistent with down-regulation of receptor densities. After a single exposure to sucrose, we found decreased binding of [11C]carfentanil in nucleus accumbens and cingulate cortex, consistent with opioid release. The lower availability of opioid and dopamine receptors may explain the addictive potential associated with intake of sucrose.
Highlights
Excessive sucrose consumption elicits addiction-like craving that may underpin the obesity epidemic
To analyze the changes occurring after the first sucrose exposure in five minipigs compared to baseline, and one day after the 12th sucrose access in seven minipigs compared to baseline, we used permutation theory and non-regionally restricted whole-brain analysis, the preferred method for samples of this size[14]
In the five minipigs imaged with [11C]carfentanil at baseline and immediately after the first sucrose exposure, we found significantly reduced tracer binding in the anterior cingulate cortex and the nucleus accumbens in response to sucrose, shown in color in Fig. 2, indicating p < 0.05
Summary
Excessive sucrose consumption elicits addiction-like craving that may underpin the obesity epidemic. We investigated the effects of sucrose using PET imaging with [11C] carfentanil (μ-opioid receptor agonist) and [11C]raclopride (dopamine D2/3 receptor antagonist) in seven female anesthetized Göttingen minipigs. The lower availability of opioid and dopamine receptors may explain the addictive potential associated with intake of sucrose. As the homeostatic regulation alone cannot account for the current rise in obesity, it is mandatory to test the effect on brain mechanisms of reward and pleasure of the addictive properties of highly palatable food. Some findings are at variance with this claim due to difficulties in separating non-palatable food consumption from hedonic food responses, and in determining the addictive ingredient in processed food, as well as the different mechanisms by which food alters brain circuitry through natural pathways[6]. We test the claim that sucrose leads to opioid and dopamine release that lowers the availability of μOR and DA D2/3 receptors. We tested the relationship between the changes in receptor availability of the two tracers
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