Gender specific effects on human eating have been previously reported. Here we investigated sex-based differences in neural activation via whole-brain blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) in response to high energy-dense (high-ED) vs. low-ED visual and auditory food cues in obese men vs. women in both fed and fasted states. The results show that in response to high vs. low ED foods in the fed state, obese men (vs. women), had greater activation in brain areas associated with motor control regions (e.g. supplementary motor areas) whereas women showed greater activation in cognitive-related regions. When fasted, obese men had greater activation in a visual-attention region whereas obese women showed greater activation in affective and reward related processing regions (e.g. caudate). Overall the results support our a priori hypothesis that obese women (vs. men) have greater neural activation in regions associated with cognition and emotion-related brain regions. These findings may improve our understanding of sex specific differences among obese individuals in eating behavior.

Reductions in mesolimbic responsivity have been noted following Roux-en-Y gastric bypass (RYGB; Ochner et al., 2011a). Given potential for postoperative increases in postprandial gut (satiety) peptides to affect mesolimbic neural responsivity, we hypothesized that: 1) post RYGB changes in mesolimbic responsivity would be greater in the fed relative to the fasted state and; 2) fasted vs. fed state differences in mesolimbic responsivity would be greater post- relative to pre- surgery. fMRI was used to asses neural responsivity to high- and low-calorie food cues in five women 1mo pre- and 1mo post-RYGB. Scans were repeated in fasted and fed states. Significant post RYGB decreases in the insula, ventromedial prefrontal cortex (vmPFC) and dorsolateral prefrontal cortex (dlPFC) responsivity were found in the fasted state. These changes were larger than neural changes in the fed state, which were non-significant. Preoperatively, fasted vs. fed differences in neural responsivity were greater in the precuneus, with large but nonsignificant clusters in the vmPFC and dlPFC. Postoperatively, however, no fasted vs. fed differences in neural responsivity were noted. Results were opposite to that predicted and appear inconsistent with the initial hypothesis that postoperative increases in postprandial gut peptides are the primary driver of postoperative changes in neural responsivity.

Body Adiposity Index (BAI), a new surrogate measure of body fat (hip circumference/[height1.5 -18]), has been proposed as an alternative to BMI. We compared BAI with BMI, and each of them with laboratory measures of body fat-derived from bioimpedance analysis (BIA), air displacement (ADP), and dual-energy x-ray absorptiometry (DXA) in clinically severe obese (CSO) participants. Nineteen pre-bariatric surgery CSO, non-diabetic women were recruited (age=32.6±7.7 SD; BMI=46.5±9.0 kg/m2). Anthropometrics and body fat percentage (% fat) were determined from BIA, ADP, and DXA. Scatter plots with lines of equality and Bland-Altman plots were used to compare BAI and BMI with % fat derived from BIA, ADP, and DXA. BAI and BMI correlated highly with each other (r=0.90, p<0.001). Both BAI and BMI correlated significantly with % fat from BIA and ADP. BAI, however, did not correlate significantly with % fat from DXA (r=0.42, p=0.08) whereas BMI did (r=0.65, p=0.003). BMI was also the single best predictor of % fat from both BIA (r2=0.80, p<0.001) and ADP (r2=0.65, p<0.001). The regression analysis showed that the standard error of the estimate (SEE) or residual error around the regression lines was greater for BAI comparisons than for BMI comparisons with BIA, ADP, and DXA. Consistent with this, the Bland and Altman plots indicated wider 95% confidence intervals for BAI difference comparisons than for BMI difference comparisons with their respective means with BIA, ADP, and DXA. Thus, BAI does not appear to be an appropriate proxy for BMI in clinically severe obese (CSO) women.