Bariatric surgery in obese patients reduced resting connectivity of brain regions involved with self‐referential processing

Abstract

Obese individuals exhibit brain alterations of resting-state functional connectivity (RSFC) integrity of resting-state networks (RSNs) related to food intake. Bariatric surgery is currently the most effective treatment for combating morbid obesity. How bariatric surgery influences neurocircuitry is mostly unknown. Functional connectivity density (FCD) mapping was employed to calculate local (lFCD)/global (gFCD) voxelwise connectivity metrics in 22 obese participants who underwent functional magnetic resonance imaging before and 1 month after sleeve gastrectomy (SG), and in 19 obese controls (Ctr) without surgery but tested twice (baseline and 1-month later). Two factor (group, time) repeated measures ANOVA was used to assess main and interaction effects in lFCD/gFCD; regions of interest were identified for subsequent seed to voxel connectivity analyses to assess resting-state functional connectivity and to examine association with weight loss. Bariatric surgery significantly decreased lFCD in VMPFC, posterior cingulate cortex (PCC)/precuneus, and dorsal anterior cingulate cortex (dACC)/dorsomedial prefrontal cortex (DMPFC) and decreased gFCD in VMPFC, right dorsolateral prefrontal cortex (DLPFC) and right insula (p < .05). lFCD decreased in VMPFC and PCC/precuneus correlated with reduction in BMI after surgery. Seed to voxel connectivity analyses showed the VMPFC had stronger connectivity with left DLPFC and weaker connectivity with hippocampus/parahippocampus, and PCC/precuneus had stronger connectivity with right caudate and left DLPFC after surgery. Bariatric surgery significantly decreased FCD in regions involved in self-referential processing (VMPFC, DMPFC, dACC, and precuneus), and interoception (insula), and changes in VMPFC/precuneus were associated with reduction in BMI suggesting a role in improving control of eating behaviors following surgery.

Laparoscopic sleeve gastrectomy induces sustained changes in gray and white matter brain volumes and resting functional connectivity in obese patients

“…Numerous RS-fMRI studies revealed LSG induced profound baseline changes in eating-related neural circuitry, including the INS and PCC [13]. Studies from our group using seed-based correlation analyses showed enhanced RSFC between the PCC/precuneus and right caudate/left dorsolateral prefrontal cortex postLSG and between the HIPP and INS [14,15]. A partial reversal of PCC dysfunction and altered brain activity (INS) after body mass index (BMI) reduction have also been reported [14,16].…”

“…Studies from our group using seed-based correlation analyses showed enhanced RSFC between the PCC/precuneus and right caudate/left dorsolateral prefrontal cortex postLSG and between the HIPP and INS [14,15]. A partial reversal of PCC dysfunction and altered brain activity (INS) after body mass index (BMI) reduction have also been reported [14,16]. Bariatric surgery also decreased RSFC within the default-mode network (DMN) [12,13].…”

“…PostLSG there were sustained increases in WM volumes at 1 and 3 months in PHIPP, which is critical for memory encoding and retrieval. PHIPP is also implicated in food craving, the physiologic state of hunger, when motivationally relevant food objects are shown [14], and when tasting a liquid meal. Several neuroimaging studies showed increased PHIPP activation to high-energy visual food cues and decreased PHIPP activation after weight loss surgery [31].…”

“…Those aforementioned studies provided evidence that bariatric surgery (i.e., LSG) promoted alterations in both brain structures and function along with concomitant weight loss [4,11,14,15]. It remains unclear whether LSG-induced changes in RSFC are associated with structural alterations.…”

History of early life adversity is associated with increased food addiction and sex‐specific alterations in reward network connectivity in obesity

“…Based on previous research , regions of interest were restricted to core regions of the ‘reward network’ (basal ganglia: caudate, pallidum, nucleus accumbens and brainstem, including the substantia nigra [SN] and ventral tegmental area [VTA]) and the extended reward network, which includes the ‘emotional regulation network’ (amygdala, hippocampus, subgenual anterior cingulate cortex and anterior cingulate cortex [ACC]), the ‘salience network’ (anterior insula [aINS] and anterior mid‐cingulate cortex), the ‘executive control network’ (dorsolateral prefrontal cortex [dlPFC], ventrolateral prefrontal cortex [vlPFC], medial prefrontal cortex [mPFC] and orbital frontal gyrus [OFG]) and the ‘somatosensory network’ (putamen and thalamus) (Table , which contains a list of the regions and their Atlas labels).…”