Abstract
Intra-cortical myelin is a myelinated part of the cerebral cortex that is responsible for the spread and synchronization of neuronal activity in the cortex. Recent animal studies have established a link between obesity and impaired oligodendrocyte maturation vis-à-vis cells that produce and maintain myelin; however, the association between obesity and intra-cortical myelination remains to be established. To investigate the effects of obesity on intra-cortical myelin in living humans, we employed a large, demographically well-characterized sample of healthy young adults drawn from the Human Connectome Project (n = 1066). Intra-cortical myelin was assessed using a novel T1-w/T2-w ratio method. Linear regression analysis was used to investigate the association between body mass index (BMI), an indicator of obesity, and intra-cortical myelination, adjusting for covariates of no interest. We observed BMI was related to lower intra-cortical myelination in regions previously identified to be involved in reward processing (i.e., medial orbitofrontal cortex, rostral anterior cingulate cortex), attention (i.e., visual cortex, inferior/middle temporal gyrus), and salience detection (i.e., insula, supramarginal gyrus) in response to viewing food cues (corrected p < 0.05). In addition, higher BMIs were associated with more intra-cortical myelination in regions associated with somatosensory processing (i.e., the somatosensory network) and inhibitory control (i.e., lateral inferior frontal gyrus, frontal pole). These findings were also replicated after controlling for key potential confounding factors including total intracranial volume, substance use, and fluid intelligence. Findings suggested that altered intra-cortical myelination may represent a novel microstructure-level substrate underlying prior abnormal obesity-related brain neural activity, and lays a foundation for future investigations designed to evaluate how living habits, such as dietary habit and physical activity, affect intra-cortical myelination.
Highlights
The abundance of accessible, high-energy palatable food has contributed to a change in how people relate to food, and is most commonly manifested as an increase in obesity [1]
Previous studies investigating the association between food-related cue-induced brain activity and obesity have consistently found abnormal neural activity in an assumed network of brain reward processing areas, including the ventral striatum and orbitofrontal cortex (OFC) regions [3,4,5,6,7] as well as areas involved in visual attention and salience detection [7,8,9,10], and somatosensory processing [4,6,8]
We found that most of the associations between body mass index (BMI) and intra-cortical myelin observed without adjusting for Hemoglobin A1C (HbA1c) remained significant when adjusting for HbA1c, except that right inferior temporal gyrus were not significantly related to BMI
Summary
The abundance of accessible, high-energy palatable food has contributed to a change in how people relate to food, and is most commonly manifested as an increase in obesity [1]. Previous studies investigating the association between food-related cue-induced brain activity and obesity have consistently found abnormal neural activity in an assumed network of brain reward processing areas, including the ventral striatum and orbitofrontal cortex (OFC) regions [3,4,5,6,7] as well as areas involved in visual attention and salience detection (e.g., occipital lobe, insula, supramarginal gyrus, precuneus, middle/inferior temporal gyrus) [7,8,9,10], and somatosensory processing (e.g., somatosensory cortex) [4,6,8]. In terms of underlying micro-structural bases of obesity, it remains unclear whether abnormal neural activities in these regions are dependent on defects or changes in levels of myelin
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