scholarly journals Chronic spinal cord changes in a high-fat diet-fed male rat model of thoracic spinal contusion

2017 ◽  
Vol 49 (9) ◽  
pp. 519-529 ◽  
Author(s):  
Redin A. Spann ◽  
William J. Lawson ◽  
Raymond J. Grill ◽  
Michael R. Garrett ◽  
Bernadette E. Grayson
Keyword(s):  
Metabolic Disease ◽  
Spinal Cord ◽  
High Fat Diet ◽  
Immune Cell ◽  
Male Rat ◽  
High Fat ◽  
Thoracic Spinal ◽  
Increased Risk ◽  
Cord Injury ◽  
The Impact

Individuals that suffer injury to the spinal cord can result in long-term, debilitating sequelae. Spinal cord-injured patients have increased risk for the development of metabolic disease, which can further hinder the effectiveness of treatments to rehabilitate the cord and improve quality of life. In the present study, we sought to understand the impact of high-fat diet (HFD)-induced obesity on spinal cord injury (SCI) by examining transcriptome changes in the area of the injury and rostral and caudal to site of damage 12 wk after injury. Adult, male Long-Evans rats received either thoracic level contusion of the spinal cord or sham laminectomy and then were allowed to recover on normal rat chow for 4 wk and further on HFD for an additional 8 wk. Spinal cord tissues harvested from the rats were processed for Affymetrix microarray and further transcriptomic analysis. Diverse changes in gene expression were identified in the injured cord in genes such as MMP12, APOC4, GPNMB, and IGF1 and 2. The greatest signaling changes occurred in pathways involved in cholesterol biosynthesis and immune cell trafficking. Together, the cord changes in the chronically obese rat following thoracic SCI reveal further potential targets for therapy. These could be further explored as they overlap with genes involved in metabolic disease.

What do we currently know about thoracic spinal cord injury recovery and outcomes? A systematic review

2012 ◽  
Vol 17 (Suppl1) ◽  
pp. 52-64 ◽  
Author(s):  
Richard J. Bransford ◽  
Jens R. Chapman ◽  
Andrea C. Skelly ◽  
Ellen M. VanAlstyne
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injuries ◽  
Poor Quality ◽  
Pulmonary Complications ◽  
Level Of Evidence ◽  
Thoracic Spinal Cord ◽  
Strength Of Evidence ◽  
Thoracic Spinal ◽  
Cord Injury ◽  
The Impact

Object The purpose of this paper was to systematically review and critically appraise the evidence for whether there are differences in outcomes or recovery after thoracic spinal cord injuries (SCIs) based on the spinal level, the timing of intervention, or cause of SCI. Methods Systematic searches were conducted using PubMed/MEDLINE through January 5, 2012. From 486 articles identified, 10 included data on the population of interest. Included studies were assigned a level of evidence (LOE) rating based on study quality, and an overall strength of evidence was assessed. To estimate the effect of injury level on patient outcomes, the relative risk and risk difference were calculated when data were available. Results From 486 citations identified, 3 registry studies and 7 retrospective cohort studies met the inclusion criteria. All were rated as being of poor quality (LOE III). Limited literature exists on the epidemiology of traumatic and nontraumatic SCI. Few studies evaluated outcomes based on SCI level within the thoracic spine. Pulmonary complications and thromboembolic events were less common in persons with lower thoracic SCI (T7–12) than in those with higher thoracic SCI (T1–6) in 2 large studies, but no differences were found in functional outcomes in 4 smaller studies. Patients undergoing earlier surgery (< 72 hours) may have fewer ventilator, ICU, and hospital days than those undergoing later surgery. One small study of SCI during repair of aortic aneurysm compared with traumatic SCI reported similar outcomes for both groups. There are substantial deficiencies in the scientific literature on thoracic SCI in regard to assessment, outcomes ratings, and effectiveness of therapy. Conclusions The overall strength of evidence for all outcomes reported is low. Definitive conclusions should not be drawn regarding the prognosis for outcome and recovery after thoracic SCI. From a physiological standpoint, additional methodologically rigorous studies that take into consideration various levels of injury in more anatomically and physiologically relevant form are needed. Use of validated, comprehensive outcomes tools are important to improve our understanding of the impact of thoracic SCI and aid in examining factors in recovery from thoracic SCI.

scholarly journals The Impact of Maternal High-Fat Diet on Bone Microarchitecture in Offspring

2021 ◽  
Vol 8 ◽  
Author(s):  
Emma J. Buckels ◽  
Scott M. Bolam ◽  
Mei Lin Tay ◽  
Brya G. Matthews
Keyword(s):  
Bone Health ◽  
High Fat Diet ◽  
Maternal Obesity ◽  
Bone Microarchitecture ◽  
Later Life ◽  
Reproductive Age ◽  
High Fat ◽  
Increased Risk ◽  
Increase Fracture Risk ◽  
The Impact

The incidence of obesity in women of reproductive age has significantly increased over the past 100 years. There is a well-established connection between maternal obesity during pregnancy and an increased risk of developing non-communicable cardiometabolic diseases in her offspring. This mini-review focuses on evidence examining the effect of maternal high-fat diet (HFD) on skeletal development and bone health in later life in offspring. The majority of rodent studies indicate that maternal HFD generally negatively affects both embryonic bone development and bone volume in adult animals. Details surrounding the mechanisms of action that drive changes in the skeleton in offspring remain unclear, although numerous studies suggest that some effects are sex-specific. Human studies in this area are limited but also suggest that HFD during pregnancy may impair bone formation and increase fracture risk during childhood. Given the consequences of low bone mass and deranged bone microarchitecture for offspring, advances in our understanding of the developmental origins of bone health is critical in the battle against osteoporosis.

scholarly journals The Effects of Brain Serotonin Deficiency on Responses to High Fat Diet in Female Mice

2021 ◽  
Vol 15 ◽  
Author(s):  
Shama N. Huq ◽  
Allison K. Warner ◽  
Kerry Buckhaults ◽  
Benjamin D. Sachs
Keyword(s):  
High Fat Diet ◽  
Tryptophan Hydroxylase ◽  
Forced Swim Test ◽  
Brain Serotonin ◽  
Dependent Manner ◽  
Depression And Anxiety ◽  
High Fat ◽  
Anxiogenic Effect ◽  
Increased Risk ◽  
The Impact

Clinical studies have reported an increased risk of depression and anxiety disorders among individuals who are obese, and women are more likely than men to suffer from depression, anxiety, and obesity. However, the effects of obesity-promoting diets on depression- and anxiety-like behavior remain controversial. A recent study from our group used the tryptophan hydroxylase 2 (R439H) knock-in mouse line to evaluate the impact of genetic brain serotonin (5-HT) deficiency on behavioral responses to high fat diet (HFD) in male mice. That study indicated that chronic exposure to HFD induced pro-anxiety-like effects in the open field test and antidepressant-like effects in the forced swim test in wild-type males. Interestingly, the antidepressant-like effect of HFD, but not the anxiogenic effect, was blocked by brain 5-HT deficiency in males. The current work sought to repeat these studies in females. Our new data suggest that females are less susceptible than males to HFD-induced weight gain and HFD-induced alterations in behavior. In addition, the effects of chronic HFD on the expression of inflammation-related genes in the hippocampus were markedly different in females than we had previously reported in males, and HFD was shown to impact the expression of several inflammation-related genes in a genotype-dependent manner. Together, our findings highlight the importance of brain 5-HT and sex in regulating behavioral and molecular responses to HFD. Our results may have important implications for our understanding of the clinically observed sex differences in the consequences of obesity.

scholarly journals High fat diet worsens pathology and impairment in an Alzheimer’s mouse model, but not by synergistically decreasing cerebral blood flow

2019 ◽  
Author(s):  
Oliver Bracko ◽  
Lindsay K. Vinarcsik ◽  
Jean C. Cruz Hernández ◽  
Nancy E. Ruiz-Uribe ◽  
Mohammad Haft-Javaherian ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Fat Diet ◽  
Brain Inflammation ◽  
Neutrophil Adhesion ◽  
High Fat ◽  
Increased Risk ◽  
The Impact

AbstractObesity is linked to increased risk for and severity of Alzheimer’s disease (AD). Cerebral blood flow (CBF) reductions are an early feature of AD and are also linked to obesity. We showed that non-flowing capillaries, caused by adhered neutrophils, underlie the CBF reduction in mouse models of AD. Because obesity could exacerbate the vascular inflammation likely underlying this neutrophil adhesion, we tested links between obesity and AD by feeding APP/PS1 mice a high fat diet (Hfd) and evaluating behavioral, physiological, and pathological changes. We found trends toward poorer memory performance in APP/PS1 mice fed a Hfd, impaired social interactions with either APP/PS1 genotype or a Hfd, and synergistic impairment of sensory-motor function in APP/PS1 mice fed a Hfd. The Hfd led to increases in amyloid-beta monomers and plaques in APP/PS1 mice, as well as increased brain inflammation. These results agree with previous reports showing obesity exacerbates AD-related pathology and symptoms in mice. We used a crowd-sourced, citizen science approach to analyze imaging data to determine the impact of the APP/PS1 genotype and a Hfd capillary stalling and CBF. Surprisingly, we did not see an increase in the number of non-flowing capillaries or a worsening of the CBF deficit in APP/PS1 mice fed a Hfd as compared to controls, suggesting capillary stalling is not a mechanistic link between a Hfd and increased severity of AD in mice. Reducing capillary stalling by blocking neutrophil adhesion improved CBF and short-term memory function in APP/PS1 mice, even when fed a Hfd.Significance statementObesity, especially in mid-life, has been linked to increased risk for and severity of Alzheimer’s disease. Here, we show that blocking adhesion of white blood cells leads to increases in brain blood flow that improve cognitive function, regardless of whether mice are obese or not.

Non-Fasting Factor VII Coagulant Activity (FVII:C) Increased by High-Fat Diet

1994 ◽  
Vol 71 (06) ◽  
pp. 755-758 ◽  
Author(s):  
E M Bladbjerg ◽  
P Marckmann ◽  
B Sandström ◽  
J Jespersen
Keyword(s):  
High Fat Diet ◽  
Fat Content ◽  
Factor Vii ◽  
Amidolytic Activity ◽  
High Fat ◽  
Low Fat Diet ◽  
Increased Risk ◽  
Coagulant Activity ◽  
High Fat Diets ◽  
Fat Diets

SummaryPreliminary observations have suggested that non-fasting factor VII coagulant activity (FVII:C) may be related to the dietary fat content. To confirm this, we performed a randomised cross-over study. Seventeen young volunteers were served 2 controlled isoenergetic diets differing in fat content (20% or 50% of energy). The 2 diets were served on 2 consecutive days. Blood samples were collected at 8.00 h, 16.30 h and 19.30 h, and analysed for triglycerides, FVII coagulant activity using human (FVII:C) or bovine thromboplastin (FVII:Bt), and FVII amidolytic activity (FVIPAm). The ratio FVII:Bt/FVII:Am (a measure of FVII activation) increased from fasting levels on both diets, but most markedly on the high-fat diet. In contrast, FVII: Am (a measure of FVII protein) tended to decrease from fasting levels on both diets. FVII:C rose from fasting levels on the high-fat diet, but not on the low-fat diet. The findings suggest that high-fat diets increase non-fasting FVII:C, and consequently may be associated with increased risk of thrombosis.

Maternal High-Fat Diet Persistently Alters Bone Marrow Immune Cell Proportions and Function in a Nonhuman Primate Model

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 222-OR
Author(s):  
MICHAEL J. NASH ◽  
TAYLOR K. SODERBORG ◽  
RACHEL C. JANSSEN ◽  
ERIC M. PIETRAS ◽  
JACOB E. FRIEDMAN
Keyword(s):  
Bone Marrow ◽  
Nonhuman Primate ◽  
High Fat Diet ◽  
Immune Cell ◽  
High Fat ◽  
Nonhuman Primate Model ◽  
Primate Model ◽  
And Function

Alteraciones sistémicas y metabólicas producidas por lesión medular

2019 ◽  
Vol 1 (1) ◽  
pp. 59-75
Author(s):  
Gabriel Guízar Sahagún
Keyword(s):  
Spinal Cord ◽  
Daily Living ◽  
Autonomic Function ◽  
Clinical Presentation ◽  
Scientific Literature ◽  
International Standards ◽  
Therapeutic Approaches ◽  
Cord Injury ◽  
Life Threatening ◽  
The Impact

Besides the well-known loss of motor and sensory capabilities, people with spinal cord injury (SCI) experience a broad range of systemic and metabolic abnormalities including, among others, dysfunction of cardiovascular, respiratory, gastrointestinal, urinary, and endocrine systems. These alterations are a significant challenge for patients with SCI because such disorders severely interfere with their daily living and can be potentially life-threatening. Most of these disorders are associated with impairment of regulation of the autonomic nervous system, arising from disruption of connections between higher brain centers and the spinal cord caudal to the injured zone. Thus, the higher and more complete the lesion, the greater the autonomic dysfunction and the severity of complications.This article summarizes the medical scientific literature on key systemic and metabolic alterations derived of SCI. It provides information primarily focused on the pathophysiology and clinical presentation of these disorders, as well as some guides to prevent and alleviate such complications. Due to the impact of these alterations, this topic must be a priority and diffuse to those involved with the care of people with SCI, including the patient himself/herself. We consider that any collaborative effort should be supported, like the development of international standards, to evaluate autonomic function after SCI, as well as the development of novel therapeutic approaches.

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