Reorganization of brain connectivity in obesity

Abstract

Global brain connectivity (GBC) identifies regions of the brain, termed "hubs," which are densely connected and metabolically costly, and have a wide influence on brain function. Since obesity is associated with central and peripheral metabolic dysfunction we sought to determine if GBC is altered in obesity. Two independent fMRI data sets were subjected to GBC analyses. The first data set was acquired while participants (n = 15 healthy weight and 15 obese) tasted milkshake and the second with participants at rest (n = 33 healthy weight and 28 obese). In the resting state and during milkshake consumption GBC is consistently decreased in the ventromedial and ventrolateral prefrontal cortex, insula and caudate nucleus, and increased in brain regions belonging to the dorsal attention network including premotor areas, superior parietal lobule, and visual cortex. During milkshake consumption, but not at rest, additional decreases in GBC are observed in feeding-related circuitry including the insula, amygdala, anterior hippocampus, hypothalamus, midbrain, brainstem and somatomotor cortex. Additionally, GBC differences were not accounted for by age. These results demonstrate that obesity is associated with decreased GBC in prefrontal and feeding circuits and increased GBC in the dorsal attention network. We therefore conclude that global brain organization is altered in obesity to favor networks important for external orientation over those monitoring homeostatic state and guiding feeding decisions. Furthermore, since prefrontal decreases are also observed at rest in obese individuals future work should evaluate whether these changes are associated with neurocognitive impairments frequently observed in obesity and diabetes. Hum Brain Mapp 38:1403-1420, 2017. © 2016 Wiley Periodicals, Inc.

Higher body mass index is associated with reduced posterior default mode connectivity in older adults

“…In our large cohort, we did not observe previously reported increased putamen and insula connectivity [Hogenkamp et al, ], decreased insula–anterior cingulate cortex (ACC) connectivity [Moreno‐Lopez et al, ], increased salience network connectivity [Figley et al, ; Garcia‐Garcia et al, ], reduced temporal lobe network connectivity [Kullmann et al, ] or increased DMN connectivity [Kullmann et al, ; Legget et al, ; Tregellas et al, ] with higher BMI. Similar to our results, one study reported reduced precuneus connectivity for obese compared with lean participants, although the results might have been confounded by the significant age difference between groups [Geha et al, ]. In a recent study with 496 participants, DMN cohesiveness has been shown to be reduced in young, obese compared with lean individuals, with highest effect size found for the posterior DMN component which is in line with our results.…”

Early maturational emergence of adult-like emotional reactivity and anxiety after brief exposure to an obesogenic diet

“…The PFC and amygdala undergo striking structural changes during adolescence (Jalbrzikowski et al, 2017), providing a biological basis that may underlie their unique vulnerability to the disruptive effects of obesity and the consumption of diets rich in saturated fats and sugars. Paralleling clinical data in humans (Geha et al, 2017;Riederer et al, 2016), we showed that DIO rats exhibit significant and partly irreversible microstructural alterations in mPFC regions and amygdalar nuclei associated with fear learning and fear extinction (Vega-Torres et al, 2018). The impact of obesogenic diets on PFC and BLA neuroplasticity is supported by studies showing reduced dendritic spine density in the PFC (Dingess et al, 2017) and dendritic length in the basal arbors of the BLA (Janthakhin et al, 2017) in rats that consume obesogenic diets rich in fats.…”

Developmental regulation of fear memories by an obesogenic high-saturated fat/high-sugar diet

“…The PFC and amygdala undergo striking structural changes during adolescence (Jalbrzikowski et al, 2017), providing a biological basis that may underlie their unique vulnerability to the disruptive effects of obesity and the consumption of diets rich in saturated fats and sugars. Paralleling clinical data in humans (Geha et al, 2017;Riederer et al, 2016), we showed that DIO rats exhibit significant and partly irreversible microstructural alterations in the mPFC and amygdala regions associated with fear learning and fear extinction (Vega-Torres et al, 2018). The impact of obesogenic diets on PFC and BLA neuroplasticity is supported by studies showing reduced dendritic spine density in the PFC (Dingess et al, 2017) and dendritic length in the basal arbors of the BLA (Janthakhin et al, 2017) in rats that consume obesogenic diets rich in fats.…”