Obesity Is Associated with Decreased  -Opioid But Unaltered XXXX Availability in the Brain.

@entity1 @entity6253 @entity28 @entity7298 @entity1633
UNASSIGNED: Neurochemical pathways involved in pathological @entity7298 and @entity28 are poorly understood. Although previous studies have shown increased  -opioid receptor ( @entity6253 ) and decreased @entity1633 (D2R) availability in addictive disorders, the role that these systems play in @entity1 @entity28 still remains unclear. We studied 13 morbidly @entity28 @entity1 [mean body mass index (BMI), 42 kg/m(2)] and 14 nonobese age-matched @entity1 , and measured brain @entity6253 and D2R availability using PET with selective radioligands [(11)C]carfentanil and [(11)C]raclopride, respectively. We also used quantitative meta-analytic techniques to pool previous evidence on the effects of @entity28 on altered D2R availability. Morbidly @entity28 subjects had significantly lower @entity6253 availability than control subjects in brain regions relevant for reward processing, including ventral striatum, insula, and thalamus. Moreover, in these areas, BMI correlated negatively with @entity6253 availability. Striatal @entity6253 availability was also negatively associated with self-reported food addiction and restrained eating patterns. There were no significant differences in D2R availability between @entity28 and nonobese subjects in any brain region. Meta-analysis confirmed that current evidence for altered D2R availability in @entity28 is only modest. Obesity appears to have unique neurobiological underpinnings in the reward circuit, whereby it is more similar to opioid addiction than to other addictive disorders. The opioid system modulates motivation and reward processing, and low  -opioid availability may promote @entity7298 to compensate decreased hedonic responses in this system. Behavioral and pharmacological strategies for recovering opioidergic function might thus be critical to curb the @entity28 epidemic.
