Diet-Induced Overweight Conditions: Effect on Brain Structure, Cognitive Function, and Neurogenesis
Obesity, a chronic condition that is currently prevalent in both developed and developing nations, is associated with pathological features that ultimately put individuals at risk for a number of negative health issues. Cognitive decline and insulin resistance are two aspects of metabolic syndrome t...
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| Main Authors: | , , , , |
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| Format: | Book Chapter |
| Language: | English |
| Published: |
IntechOpen
2023
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| Subjects: | |
| Online Access: | https://www.intechopen.com/chapters/86737 |
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| Summary: | Obesity, a chronic condition that is currently prevalent in both developed and developing nations, is associated with pathological features that ultimately put individuals at risk for a number of negative health issues. Cognitive decline and insulin resistance are two aspects of metabolic syndrome that are closely linked to neurological dysfunction during obesity. Several studies suggest that obesity is associated with regional structural changes, especially signs of cortical thinning in specific brain regions like the hippocampus, and reduced microstructural integrity of the white matter tract is associated with an overall lower academic performance. Obesity causes a loss of brain size and volume indicating a loss of neurons which leads to poor cognitive performance and reduced neurogenesis. An increase in the production of free fatty acids seen with HFD eating might result in increased oxidative stress and increased production of reactive oxygen species. The main cause of systemic inflammation in obesity is the build-up of adipose as it releases TNFα, PAI-1, CRP, IL-1β, and IL-6 which contribute to a pro-inflammatory state in the central nervous system. These elements can all lead to the central IKK/NF-B inflammatory signalling cascade being activated, which can cause a vicious inflammatory cycle that quickens and causes neurodegeneration and cognitive decline. |
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| ISBN: | 978-1-80355-909-4 |
| DOI: | 10.5772/intechopen.110610 |