Impact of High Fat Consumption on Neurological Functions after Traumatic Brain Injury in Rats

Thomson, Shannon; Chan, Yik Lung; Yi, Chenju; Wang, Baoming; Machaalani, Rita; Oliver, Brian G.; Gorrie, Catherine A.; Chen, Hui

doi:10.1089/neu.2022.0080

Cited by 5 publications

(3 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Notably, evidence suggests that pre-existing diet-induced obesity is associated with an amplification of post-TBI pro-inflammatory responses and increased microglia-altered states in several brain regions [23][24][25]. Additional studies report dietinduced exacerbations in TBI-induced cognitive decline [24,25] and central (brain) insulin resistance [26].…”

Section: Introductionmentioning

confidence: 98%

“…Activation of brain and peripheral inflammation pathways is a key pathophysiological feature in both TBI [8][9][10][11][12] and obesity [12][13][14][15][16][17][18][19][20] and has been implicated in the development of associated neurological dysfunction [8,21,22]. Notably, evidence suggests that pre-existing diet-induced obesity is associated with an amplification of post-TBI pro-inflammatory responses and increased microglia-altered states in several brain regions [23][24][25]. Additional studies report dietinduced exacerbations in TBI-induced cognitive decline [24,25] and central (brain) insulin resistance [26].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Interaction of high-fat diet and brain trauma alters adipose tissue macrophages and brain microglia associated with exacerbated cognitive dysfunction

Henry

Barrett

Vaida

et al. 2023

Preprint

View full text Add to dashboard Cite

Obesity increases the morbidity and mortality of traumatic brain injury (TBI). We performed a detailed analysis of transcriptomic changes in the brain and adipose tissue to examine the interactive effects between high-fat diet-induced obesity (DIO) and TBI in relation to central and peripheral inflammatory pathways, as well as neurological function. Adult male mice were fed a high-fat diet (HFD) for 12 weeks prior to experimental TBI and continuing after injury. Combined TBI and HFD resulted in additive dysfunction in the Y-Maze, novel object recognition (NOR), and Morris water maze (MWM) cognitive function tests. We also performed high-throughput transcriptomic analysis using Nanostring panels of cellular compartments in the brain and total visceral adipose tissue (VAT), followed by unsupervised clustering, principal component analysis, and IPA pathway analysis to determine shifts in gene expression programs and molecular pathway activity. Analysis of cellular populations in the cortex and hippocampus as well as in visceral adipose tissue during the chronic phase after combined TBI-HFD showed amplification of central and peripheral microglia/macrophage responses, including superadditive changes in select gene expression signatures and pathways. These data suggest that HFD-induced obesity and TBI can independently prime and support the development of altered states in brain microglia and visceral adipose tissue macrophages, including the disease-associated microglia/macrophage (DAM) phenotype observed in neurodegenerative disorders. The interaction between HFD and TBI promotes a shift toward chronic reactive microglia/macrophage transcriptomic signatures and associated pro-inflammatory disease-altered states that may, in part, underlie the exacerbation of cognitive deficits. Targeting of HFD-induced reactive cellular phenotypes, including in peripheral adipose tissue macrophages, may serve to reduce microglial maladaptive states after TBI, attenuating post-traumatic neurodegeneration and neurological dysfunction.

show abstract

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Interaction of high-fat diet and brain trauma alters adipose tissue macrophages and brain microglia associated with exacerbated cognitive dysfunction

Henry

Barrett

Vaida

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

“…Notably, evidence suggests that pre-existing diet-induced obesity is associated with an amplification of post-TBI pro-inflammatory responses and increased microglia-altered states in several brain regions [ 23 – 25 ]. Additional studies report diet-induced exacerbations in TBI-induced cognitive decline [ 24 , 25 ] and central (brain) insulin resistance [ 26 ].…”

Section: Introductionmentioning

confidence: 99%

Interaction of high-fat diet and brain trauma alters adipose tissue macrophages and brain microglia associated with exacerbated cognitive dysfunction

Henry,

Barrett,

Vaida

et al. 2024

J Neuroinflammation

View full text Add to dashboard Cite

Obesity increases the morbidity and mortality of traumatic brain injury (TBI). Detailed analyses of transcriptomic changes in the brain and adipose tissue were performed to elucidate the interactive effects between high-fat diet-induced obesity (DIO) and TBI. Adult male mice were fed a high-fat diet (HFD) for 12 weeks prior to experimental TBI and continuing after injury. High-throughput transcriptomic analysis using Nanostring panels of the total visceral adipose tissue (VAT) and cellular components in the brain, followed by unsupervised clustering, principal component analysis, and IPA pathway analysis were used to determine shifts in gene expression patterns and molecular pathway activity. Cellular populations in the cortex and hippocampus, as well as in VAT, during the chronic phase after combined TBI-HFD showed amplification of central and peripheral microglia/macrophage responses, including superadditive changes in selected gene expression signatures and pathways. Furthermore, combined TBI and HFD caused additive dysfunction in Y-Maze, Novel Object Recognition (NOR), and Morris water maze (MWM) cognitive function tests. These novel data suggest that HFD-induced obesity and TBI can independently prime and support the development of altered states in brain microglia and VAT, including the disease-associated microglia/macrophage (DAM) phenotype observed in neurodegenerative disorders. The interaction between HFD and TBI promotes a shift toward chronic reactive microglia/macrophage transcriptomic signatures and associated pro-inflammatory disease-altered states that may, in part, underlie the exacerbation of cognitive deficits. Thus, targeting of HFD-induced reactive cellular phenotypes, including in peripheral adipose tissue immune cell populations, may serve to reduce microglial maladaptive states after TBI, attenuating post-traumatic neurodegeneration and neurological dysfunction.

show abstract

The impact of body mass index changes on traumatic brain injury patients’ outcomes during hospitalization

Aminmansour,

Sameri,

Shafiei

et al. 2023

Chinese Journal of Traumatology

View full text Add to dashboard Cite

Impact of High Fat Consumption on Neurological Functions after Traumatic Brain Injury in Rats

Cited by 5 publications

References 43 publications

Interaction of high-fat diet and brain trauma alters adipose tissue macrophages and brain microglia associated with exacerbated cognitive dysfunction

Interaction of high-fat diet and brain trauma alters adipose tissue macrophages and brain microglia associated with exacerbated cognitive dysfunction

Interaction of high-fat diet and brain trauma alters adipose tissue macrophages and brain microglia associated with exacerbated cognitive dysfunction

The impact of body mass index changes on traumatic brain injury patients’ outcomes during hospitalization

Contact Info

Product

Resources

About