Abstract
ObjectiveObesity is associated with impaired inhibitory control over food intake. We hypothesized that the neural circuitry underlying inhibition of food craving would be impaired in obesity. Here we assessed whether obese men show altered brain responses during attempted cognitive inhibition of craving when exposed to food cues.MethodsSixteen obese men (32 ± 8.7 years old, BMI = 38.6 ± 7.2) were compared with 11 age-matched non-obese men (BMI 24.2 ± 2.5) using PET and FDG. Brain glucose metabolism was evaluated in a food deprived state: no food stimulation, food stimulation with no inhibition (NI), and food stimulation with attempted inhibition (AI), each on a separate day. Individualized favorite food items were presented prior to and after FDG injection for 40 min. For AI, participants were asked to attempt to inhibit their desire for the food presented. Self-reports for hunger and food desire were recorded.ResultsFood stimulation compared with no stimulation increased glucose metabolism in inferior and superior frontal gyrus, default mode network and cerebellum, in both groups. For both groups, AI compared with NI-suppressed metabolism in right subgenual anterior cingulate, orbitofrontal areas, bilateral insula, and temporal gyri. There was a stimulation-by-group interaction effect in obese (but not in non-obese) men showing increased metabolism in pregenual anterior cingulate cortex (pgACC) and caudate during AI relative to NI. Changes in the food desire from NI to AI correlated negatively with changes in metabolism in pgACC/caudate in obese but not in non-obese men.ConclusionsObese men showed higher activation in pgACC/caudate, which are regions involved with self-regulation and emotion/reward during AI. Behavioral associations suggest that successful AI is an active process requiring more energy in obese but not in non-obese men. The additional required effort to increase cognitive control in response to food stimulation in obese compared with non-obese men may contribute to their uncontrolled eating behavior.
Highlights
Supplementary information The online version of this article contains supplementary material, which is available to authorized users.Bethesda, MD 20892, USAObesity is associated with significant increases in morbidity and mortality, highlighting the urgency for understanding the processes contributing to this epidemic [1, 2]
We previously showed that the desire for food during presentation of palatable food stimuli was associated with striatal dopamine (DA) release, measured using positron emission tomography (PET) with [11C]raclopride, a radiotracer whose binding is sensitive to changes in extracellular DA
We previously reported on a PET study in normal weight participants in whom we measured regional brain glucose metabolic responses when exposed to appealing food both when directed to suppress the food desire and when exposed to the food but with no inhibition (NI) [12]
Summary
We previously showed that the desire for food during presentation of palatable food stimuli was associated with striatal dopamine (DA) release, measured using positron emission tomography (PET) with [11C]raclopride, a radiotracer whose binding is sensitive to changes in extracellular DA. This finding is consistent with DA’s role in modulating the motivation for food [6], which is mediated by its regulation of striato-cortical circuits involved with drive, salience attribution, and inhibitory control [7, 8]. A recent fMRI study using the blood oxygen level dependent signal showed that obese subjects activated striatum and OFC as well as insula (a brain region involved with interoception for food signals that is innervated by DA terminals) while viewing pictures of high-caloric food [10]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
