Alterations in Functional and Structural Connectivity of Basal Ganglia Network in Patients with Obesity.

Obesity is related to overconsumption of high-calorie (HiCal) food, which is modulated by brain reward and inhibitory control circuitries. The basal ganglia (BG) are a key set of nuclei within the reward circuitry, but obesity-associated functional and structural abnormalities of BG have not been well studied. Resting-state functional MRI with independent component analysis (ICA) and probabilistic tractography were employed to investigate differences in BG-related functional-(FC) and structural connectivity (SC) between 32 patients with obesity (OB) and 35 normal-weight (NW) participants. Compared to NW, OB showed significantly lower FC strength in the caudate nucleus within the BG network, and seed-based FC analysis showed lower FC between caudate and dorsolateral prefrontal cortex (DLPFC), which was negatively correlated with craving for HiCal food cues. Further SC analysis revealed that OB showed lower SC than NW between left caudate and left DLPFC as measured with fractional anisotropy (FA). Alterations in FC and SC between caudate and DLPFC in obese patients, which highlights the role of BG network in modulating the balance between reward and inhibitory-control.

Resting activity of the hippocampus and amygdala in obese individuals predicts their response to food cues.

Obese individuals exhibit brain functional abnormalities in multiple regions implicated in reward/motivation, emotion/memory, homeostatic regulation, and executive control when exposed to food cues and during rest. However, it remains unclear whether abnormal brain responses to food cues might account for or relate to their abnormal activity in resting state. This information would be useful for understanding the neural mechanisms behind hyperactive responses to food cues, a critical marker of obesity. Resting-state functional magnetic resonance imaging (RS-fMRI) and a cue-reactivity fMRI task with high- (HiCal) and low-caloric (LoCal) food cues were employed to investigate brain baseline activity and food cue-induced activation differences in 44 obese participants (OB), in 37 overweight participants (OW), and in 37 normal weight (NW) controls. One-way analyses of variance showed there was a group difference in the left hippocampus/amygdala activity during resting state and during food-cue stimulation (pFWE < 0.05); post-hoc tests showed the OB group had both greater basal activity and greater food cue-induced activation than the OW and NW groups; OW had higher activity in the hippocampus/amygdala than the NW group, which was only significant during resting state. In the OB group, resting-state activity in the left hippocampus/amygdala was positively correlated with activation induced by HiCal food cues, and both of these measures correlated with body mass index (BMI). Mediation analysis showed that the relationship between BMI and hippocampus/amygdala response to HiCal food cues was mediated by their resting-state activity. These findings suggest a close association between obesity and brain functional abnormality in the hippocampus/amygdala. They also indicate that resting-state activity in the hippocampus/amygdala may impact these regions' responses to food cues.

Abnormalities in the thalamo-cortical network in patients with functional constipation.

Functional constipation (FCon) is a common functional gastrointestinal disorder (FGID); neuroimaging studies have shown brain functional abnormalities in thalamo-cortical regions in patients with FGID. However, association between FCon and topological characteristics of brain networks remains largely unknown. We employed resting-state functional magnetic resonance imaging (RS-fMRI) and graph theory approach to investigate functional brain topological organization in 42 patients with FCon and 41 healthy controls (HC) from perspectives of global, regional and modular levels. Results showed patients with FCon had a significantly lower normalized clustering coefficient and small-worldness, implying decreased brain functional connectivity. Regions showed altered nodal degree and efficiency mainly located in the thalamus, rostral anterior cingulate cortex (rACC), and supplementary motor area (SMA), which are involved in somatic/sensory, emotional processing and motor-control. For the modular analysis, thalamus, rACC and SMA had an aberrant within-module nodal degree and nodal efficiency, and thalamus-related network exhibited abnormal interaction with the limbic network (amygdala and hippocampal gyrus). Nodal degree in the thalamus was negatively correlated with difficulty of defecation, and nodal degree in the rACC was negatively correlated with sensation of incomplete evacuation. These findings indicated that FCon was associated with abnormalities in the thalamo-cortical network.

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

BACKGROUND: Obesity is associated with decreased brain gray- (GM) and white-matter (WM) volumes in regions. Laparoscopic sleeve gastrectomy (LSG) is an effective bariatric surgery associated with neuroplastic changes in patients with obesity at 1 month postLSG. OBJECTIVE: To investigate whether LSG can induce sustained neuroplastic recovery of brain structural abnormalities, and whether structural changes are accompanied by functional alterations. SETTING: University hospital, longitudinal study. METHODS: Structural magnetic resonance imaging and voxel-based morphometry analysis were employed to assess GM/WM volumes in 30 obese participants at preLSG and 1 and 3 months postLSG. One-way analysis of variance modeled time effects on GM/WM volumes, and then alterations in resting-state functional connectivity (RSFC) were assessed. RESULTS: Significant time effects on GM volumes were in caudate (F = 11.20), insula (INS; F = 10.11), posterior cingulate cortex (PCC; F = 13.32), and inferior frontal gyrus (F = 12.18), and on WM volumes in anterior cingulate cortex (F = 15.70), PCC (F = 15.56), and parahippocampus (F = 17.96, PFDR < .05). Post hoc tests showed significantly increased GM volumes in caudate (mean change ± SEM .018 ± .005 and P = .001, .031 ± .007 and P < .001), INS (.027 ± .008 and P = .003, .043 ± .009 and P < .001), and PCC (.008 ± .004 and P = .042, .026 ± .006 and P < .001), and increased WM volumes in anterior cingulate cortex (.029 ± .006 and P < .001, .041 ± .008 and P < .001), PCC (.017 ± .004 and P < .001, .032 ± .006 and P < .001), and parahippocampus (.031 ± .008 and P =.001, .075 ± .013 and P < .001) at 1 and 3 months postLSG compared with preLSG. Significant increases in GM volumes were in caudate (.013 ± .006 and P = .036), PCC (.019 ± .006 and P = .006), and inferior frontal gyrus (.019 ± .005 and P = .001), and in WM volumes in anterior cingulate cortex (.012 ± .005 and P = .028), PCC (.014 ± .006 and P = .017), and parahippocampus (.044 ± .014 and P = .003) at 3 relative to 1 month postLSG. GM volumes in INS and PCC showed a positive correlation at 1 (r = .57, P = .001) and 3 months postLSG (r = .55, P = .001). GM volume in INS and PCC were positively correlated with RSFC of INS-PCC (r = .40 and P = .03, r = .55 and P = .001) and PCC-INS (r = .37 and P = .046, r = .57 and P < .001) at 1 month postLSG. GM volume in INS was also positively correlated with RSFC of INS-PCC (r = .44, P = .014) and PCC-INS (r = .38, P = .037) at 3 months postLSG. CONCLUSION: LSG induces sustained structural brain changes, which might mediate long-term benefits of bariatric surgery in weight reduction. Associations between regional GM volume and RSFC suggest that LSG-induced structural changes contribute to RSFC changes.

Altered Interactions Among Resting-State Networks in Individuals with Obesity.

OBJECTIVE: The aim of this study was to investigate alterations in functional connectivity (FC) within and interactions between resting-state networks involved in salience, executive control, and interoception in participants with obesity (OB). METHODS: Using resting-state functional magnetic resonance imaging with independent component analysis and FC, alterations within and interactions between resting-state networks in 35 OB and 35 normal-weight controls (NW) were investigated. RESULTS: Compared with NW, OB showed reduced FC strength in the ventromedial prefrontal cortex and posterior cingulate cortex/precuneus within the default-mode network, dorsal anterior cingulate cortex within the salience network (SN), bilateral dorsolateral prefrontal cortex-angular gyrus within the frontoparietal network (FPN), and increased FC strength in the insula (INS) (Pfamilywise error < 0.0125). The dorsal anterior cingulate cortex FC strength was negatively correlated with craving for food cues, left dorsolateral prefrontal cortex FC strength was negatively correlated with Yale Food Addiction Scale scores, and right INS FC strength was positively correlated with craving for high-calorie food cues. Compared with NW, OB also showed increased FC between the SN and FPN driven by altered FC of bilateral INS and anterior cingulate cortex-angular gyrus. CONCLUSIONS: Alterations in FC within and interactions between the SN, default-mode network, and FPN might contribute to the high incentive value of food (craving), lack of control of overeating (compulsive overeating), and increased awareness of hunger (impaired interoception) in OB.

Cortical morphometry alterations in brain regions involved in emotional, motor-control and self-referential processing in patients with functional constipation.

Functional constipation (FC) is a common functional gastrointestinal disorder (FGID). Neuroimaging studies on patients with FC showed brain functional abnormalities in regions involved in emotional process modulation, somatic and sensory processing and motor control. Brain structural imaging studies in patients with FGID have also shown disease-related alterations in cortical morphometry, but whether and how FC affects brain structure remains unclear. Structural Magnetic Resonance Imaging and surface-based morphometry analysis were used to investigate the impact of FC on cortical morphometry in 29 patients with FC and 29 healthy controls (HC). Results showed that patients with FC compared to HC had significantly decreased cortical thickness in the left middle frontal gyrus (MFG), dorsomedial (DMPFC) and ventromedial prefrontal gyrus (VMPFC), right dorsal anterior cingulate cortex (dACC), left orbitofrontal cortex (OFC), posterior cingulate cortex (PCC)/precuneus, middle temporal gyrus (MTG), and supplementary motor area (SMA) (P < 0.01). Correlation analysis showed that sensation of incomplete evacuation was negatively correlated with cortical thickness in the SMA (P < 0.0001). In addition, patients with FC also had decreased cortical volume than HC in the MTG, precentral gyrus (PreCen) and precuneus/cuneus (P < 0.01), as well as decreased cortical surface area in the PreCen (P < 0.01). No correlation was found between cortical volume/surface area and behavioral measures. These findings suggest that patients with FC are associated with cortical morphometric abnormalities in brain regions implicated in somatic/motor-control, emotional processing and self-referential processing.