Dietary fructose aggravates the pathobiology of traumatic brain injury by influencing energy homeostasis and plasticity

Fructose consumption has been on the rise for the last two decades and is starting to be recognized as being responsible for metabolic diseases. Metabolic disorders pose a particular threat for brain conditions characterized by energy dysfunction, such as traumatic brain injury. Traumatic brain injury patients experience sudden abnormalities in the control of brain metabolism and cognitive function, which may worsen the prospect of brain plasticity and function. The mechanisms involved are poorly understood. Here we report that fructose consumption disrupts hippocampal energy homeostasis as evidenced by a decline in functional mitochondria bioenergetics (oxygen consumption rate and cytochrome C oxidase activity) and an aggravation of the effects of traumatic brain injury on molecular systems engaged in cell energy homeostasis (sirtuin 1, peroxisome proliferator-activated receptor gamma coactivator-1alpha) and synaptic plasticity (brain-derived neurotrophic factor, tropomyosin receptor kinase B, cyclic adenosine monophosphate response element binding, synaptophysin signaling). Fructose also worsened the effects of traumatic brain injury on spatial memory, which disruption was associated with a decrease in hippocampal insulin receptor signaling. Additionally, fructose consumption and traumatic brain injury promoted plasma membrane lipid peroxidation, measured by elevated protein and phenotypic expression of 4-hydroxynonenal. These data imply that high fructose consumption exacerbates the pathology of brain trauma by further disrupting energy metabolism and brain plasticity, highlighting the impact of diet on the resilience to neurological disorders.

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Poster 11: The Impact of Time Since Injury and Number of Injuries in Older Adults With Traumatic Brain Injury and Implications for Brain Plasticity

Archives of Physical Medicine and Rehabilitation ◽

10.1016/j.apmr.2008.08.038 ◽

2008 ◽

Vol 89 (10) ◽

pp. e11

Author(s):

Amanda Sacks ◽

Angela Yi ◽

Joshua Cantor ◽

Lisa Speilman ◽

Christaan Greer

Keyword(s):

Older Adults ◽

Traumatic Brain Injury ◽

Brain Injury ◽

Brain Plasticity ◽

The Impact ◽

Time Since Injury

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Hexarelin Signaling to PPARγin Metabolic Diseases

PPAR Research ◽

10.1155/2008/364784 ◽

2008 ◽

Vol 2008 ◽

pp. 1-9 ◽

Cited By ~ 12

Author(s):

Annie Demers ◽

Amélie Rodrigue-Way ◽

André Tremblay

Keyword(s):

Transcriptional Control ◽

Energy Homeostasis ◽

Metabolic Diseases ◽

Scavenger Receptor ◽

Peroxisome Proliferator ◽

Peroxisome Proliferator Activated Receptor ◽

Insulin Sensitizer ◽

Metabolic Functions ◽

Growth Hormone Releasing Peptides ◽

The Impact

Investigating the metabolic functions of the nuclear receptor peroxisome proliferator-activated receptorγ(PPARγ) has been extremely rewarding over the past years. Uncovering the biologic roles of PPARγand its mechanism of action has greatly advanced our understanding of the transcriptional control of lipid and glucose metabolism, and compounds such as thiazolidinediones which directly regulate PPARγhave proven to exhibit potent insulin-sensitizer effects in the treatment of diabetes. We review here recent advances on the emerging role of growth hormone releasing peptides in regulating PPARγthrough interaction with scavenger receptor CD36 and ghrelin GHS-R1a receptor. With the impact that these peptides exert on the metabolic pathways involved in lipid metabolism and energy homeostasis, it is hoped that the development of novel approaches in the regulation of PPAR functions will bring additional therapeutic possibilities to face problems related to metabolic diseases.

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The impact of traumatic brain injury on developmental functioning in children: Mild TBI at home and school

PsycEXTRA Dataset ◽

10.1037/e556572013-079 ◽

2012 ◽

Author(s):

Rosalind Case ◽

Nicola Starkey ◽

Suzanne Barker-Collo ◽

Kelly Jones

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Mild Tbi ◽

Developmental Functioning ◽

The Impact ◽

Home And School ◽

At Home

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Faculty Opinions recommendation of Prognostic value of demographic characteristics in traumatic brain injury: results from the IMPACT study.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1087001.539961 ◽

2007 ◽

Author(s):

Donald Marion

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Prognostic Value ◽

Demographic Characteristics ◽

Impact Study ◽

The Impact

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Impact of routine S100B protein assay on CT scan use in children with mild traumatic brain injury

Clinical Chemistry and Laboratory Medicine (CCLM) ◽

10.1515/cclm-2020-1293 ◽

2020 ◽

Vol 0 (0) ◽

Author(s):

Fleur Lorton ◽

Jeanne Simon-Pimmel ◽

Damien Masson ◽

Elise Launay ◽

Christèle Gras-Le Guen ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Mild Traumatic Brain Injury ◽

University Hospital ◽

S100b Protein ◽

Research Network ◽

Ct Scans ◽

Intermediate Risk ◽

Protein Assay ◽

The Impact

AbstractObjectivesTo evaluate the impact of implementing a modified Pediatric Emergency Care Applied Research Network (PECARN) rule including the S100B protein assay for managing mild traumatic brain injury (mTBI) in children.MethodsA before-and-after study was conducted in a paediatric emergency department of a French University Hospital from 2013 to 2015. We retrospectively included all consecutive children aged 4 months to 15 years who presented mTBI and were at intermediate risk for clinically important traumatic brain injury (ciTBI). We compared the proportions of CT scans performed and of in-hospital observations before (2013–2014) and after (2014–2015) implementation of a modified PECARN rule including the S100B protein assay.ResultsWe included 1,062 children with mTBI (median age 4.5 years, sex ratio [F/M] 0.73) who were at intermediate risk for ciTBI: 494 (46.5%) during 2013–2014 and 568 (53.5%) during 2014–2015. During 2014–2015, S100B protein was measured in 451 (79.4%) children within 6 h after mTBI. The proportion of CT scans and in-hospital observations significantly decreased between the two periods, from 14.4 to 9.5% (p=0.02) and 73.9–40.5% (p<0.01), respectively. The number of CT scans performed to identify a single ciTBI was reduced by two-thirds, from 18 to 6 CT scans, between 2013–2014 and 2014–2015. All children with ciTBI were identified by the rules.ConclusionsThe implementation of a modified PECARN rule including the S100B protein assay significantly decreased the proportion of CT scans and in-hospital observations for children with mTBI who were at intermediate risk for ciTBI.

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Interrupted time series design to evaluate ICD-9-CM to ICD-10-CM coding changes on trends in Colorado emergency department visits related to traumatic brain injury

Injury Epidemiology ◽

10.1186/s40621-021-00308-y ◽

2021 ◽

Vol 8 (1) ◽

Author(s):

Lauren Alexis De Crescenzo ◽

Barbara Alison Gabella ◽

Jewell Johnson

Keyword(s):

Public Health ◽

Traumatic Brain Injury ◽

Emergency Department ◽

Brain Injury ◽

Interrupted Time Series ◽

Emergency Department Visits ◽

Control And Prevention ◽

Icd 10 ◽

Ed Visits ◽

The Impact

Abstract Background The transition in 2015 to the Tenth Revision of the International Classification of Disease, Clinical Modification (ICD-10-CM) in the US led the Centers for Disease Control and Prevention (CDC) to propose a surveillance definition of traumatic brain injury (TBI) utilizing ICD-10-CM codes. The CDC’s proposed surveillance definition excludes “unspecified injury of the head,” previously included in the ICD-9-CM TBI surveillance definition. The study purpose was to evaluate the impact of the TBI surveillance definition change on monthly rates of TBI-related emergency department (ED) visits in Colorado from 2012 to 2017. Results The monthly rate of TBI-related ED visits was 55.6 visits per 100,000 persons in January 2012. This rate in the transition month to ICD-10-CM (October 2015) decreased by 41 visits per 100,000 persons (p-value < 0.0001), compared to September 2015, and remained low through December 2017, due to the exclusion of “unspecified injury of head” (ICD-10-CM code S09.90) in the proposed TBI definition. The average increase in the rate was 0.33 visits per month (p < 0.01) prior to October 2015, and 0.04 visits after. When S09.90 was included in the model, the monthly TBI rate in Colorado remained smooth from ICD-9-CM to ICD-10-CM and the transition was no longer significant (p = 0.97). Conclusion The reduction in the monthly TBI-related ED visit rate resulted from the CDC TBI surveillance definition excluding unspecified head injury, not necessarily the coding transition itself. Public health practitioners should be aware that the definition change could lead to a drastic reduction in the magnitude and trend of TBI-related ED visits, which could affect decisions regarding the allocation of TBI resources. This study highlights a challenge in creating a standardized set of TBI ICD-10-CM codes for public health surveillance that provides comparable yet clinically relevant estimates that span the ICD transition.

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