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Original Research

Reanalysis of the Obesity-Related Attenuation in the Left Dorsolateral Prefrontal Cortex Response to a Satiating Meal Using Gyral Regions-of-Interest

, MD, PhD, , PhD, , MD, PhD, , PhD, , MD & , MD
Pages 667-673 | Received 27 Jul 2009, Accepted 06 Dec 2009, Published online: 12 Jun 2013
 

Abstract

Objective: The left dorsolateral prefrontal cortex (LDLPFC), which includes the inferior (IFG), middle (MFG), and superior (SFG) frontal gyri, has been implicated in satiation. Using a voxel-based approach, we previously identified an LDLPFC region (as reported as peak voxel) in which a reduced neuronal response to a meal was associated with obesity. In this study, we sought to determine which gyri in the LDLPFC best distinguished the neuronal responses to a meal using a different statistical approach.

Methods: We reanalyzed brain responses to a meal using the hypothesis-driven region-of-interest–based (ROI) approach. Regional cerebral blood flow (rCBF), a marker of neuronal activity in the LDLPFC and its 3 gyri, was acquired in 2 conditions (hunger and after the satiating meal) using 15O-water positron emission tomography scans. rCBF was extracted and estimated using masks of the 3 gyri that were created in MRIcro and Statistical Parametric Mapping 5 software.

Results: Using the ROI approach, a satiation-related reduction in LDLPFC rCBF was observed in the obese (p  =  0.04) and tended to be significantly greater than that in lean subjects (p  =  0.07). The rCBF reduction was greater in the obese subjects than in the lean subjects in the left IFG (p  =  0.03) and MFG (p  =  0.004) after adjustment was made for age, sex, and number of voxels in these gyri, but not in the SFG (p  =  0.5).

Conclusions: Our results are consistent with those obtained by the voxel-based approach in showing the association between obesity and a satiation-related reduction in LDLPFC activity. This LDLPFC response preferentially involves the IFG and MFG. We suggest that these brain regions could be targeted by new therapeutic interventions.

This research was supported by the Intramural Research Program of the NIH, NIDDK. We are especially grateful to Dr Clifton Bogardus (Phoenix Epidemiology and Clinical Research Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Phoenix, AZ, United States) for helpful comments and suggestions.

Critical review of this manuscript by Dr Joy C. Bunt, with the Phoenix Epidemiology & Clinical Research Branch of the National Institute of Diabetes and Digestive and Kidney Diseases, NIH, is gratefully acknowledged.

We also thank the staffs of the Clinical Research Center and the Good Samaritan PET Center for technical assistance and the volunteer subjects for their participation.

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