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Subject:

SPORTS MEDICINE : MEDICAL: CONDITIONS: OBESITY : PHYSICAL EXERCISE AND FITNESS : COUNTRIES: WALES : FOOD DRINK NUTRITION DIET: DIET: POOR DIET: How Fat May Hurt the Brain, and How Exercise May Help

From:

"David P. Dillard" <[log in to unmask]>

Reply-To:

To support research in sports medicine <[log in to unmask]>

Date:

Sat, 8 Mar 2014 11:51:43 -0500

Content-Type:

TEXT/PLAIN

Parts/Attachments:

Parts/Attachments

TEXT/PLAIN (250 lines)

.

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SPORTS MEDICINE :

MEDICAL: CONDITIONS: OBESITY :

PHYSICAL EXERCISE AND FITNESS :

COUNTRIES: WALES :

FOOD DRINK NUTRITION DIET: DIET: POOR DIET:

How Fat May Hurt the Brain, and How Exercise May Help

.

.



How Fat May Hurt the Brain, and How Exercise May Help

By GRETCHEN REYNOLDS

Phys Ed

March 5, 2014, 12:01 am

New York Times

Well

http://well.blogs.nytimes.com/2014/03/05/
how-fat-may-harm-the-brain-and-how-exercise-may-help/?_php=true&_type=blogs&_r=0

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A shorter URL for the above link:

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http://tinyurl.com/q4bu9pj

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Obesity may have harmful effects on the brain, and exercise may counteract 
many of those negative effects, according to sophisticated new 
neurological experiments with mice, even when the animals do not lose much 
weight. While it's impossible to know if human brains respond in precisely 
the same way to fat and physical activity, the findings offer one more 
reason to get out and exercise.

.

It's been known for some time that obesity can alter cognition in animals. 
Past experiments with lab rodents, for instance, have shown that obese 
animals display poor memory and learning skills compared to their 
normal-weight peers. They don't recognize familiar objects or recall the 
location of the exit in mazes that they've negotiated multiple times.

.

But scientists hadn't understood how excess weight affects the brain. Fat 
cells, they knew, manufacture and release substances into the bloodstream 
that flow to other parts of the body, including the heart and muscles. 
There, these substances jump-start biochemical processes that produce 
severe inflammation and other conditions that can lead to poor health.

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Many thought the brain, though, should be insulated from those harmful 
effects. It contains no fat cells and sits behind the protective 
blood-brain barrier that usually blocks the entry of undesirable 
molecules.

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However, recent disquieting studies in animals indicate that obesity 
weakens that barrier, leaving it leaky and permeable. In obese animals, 
substances released by fat cells can ooze past the barrier and into the 
brain.

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The consequences of that seepage became the subject of new neurological 
experiments conducted by researchers at Georgia Regents University in 
Augusta and published last month in The Journal of Neuroscience.

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The complete article may be read at the URL above.

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J Neurosci. 2014 Feb 12;34(7):2618-31.
doi: 10.1523/JNEUROSCI.4200-13.2014.
Obesity elicits interleukin 1-mediated deficits in hippocampal synaptic 
plasticity.
Erion JR1, Wosiski-Kuhn M, Dey A, Hao S, Davis CL, Pollock NK, Stranahan 
AM.

Abstract

Adipose tissue is a known source of proinflammatory cytokines in obese 
humans and animal models, including the db/db mouse, in which obesity 
arises as a result of leptin receptor insensitivity. Inflammatory 
cytokines induce cognitive deficits across numerous conditions, but no 
studies have determined whether obesity-induced inflammation mediates 
synaptic dysfunction. To address this question, we used a treadmill 
training paradigm in which mice were exposed to daily training sessions or 
an immobile belt, with motivation achieved by delivery of compressed air 
on noncompliance. Treadmill training prevented hippocampal microgliosis, 
abolished expression of microglial activation markers, and also blocked 
the functional sensitization observed in isolated cells after ex vivo 
exposure to lipopolysaccharide. Reduced microglial reactivity with 
exercise was associated with reinstatement of hippocampus-dependent 
memory, reversal of deficits in long-term potentiation, and normalization 
of hippocampal dendritic spine density. Because treadmill training evokes 
broad responses not limited to the immune system, we next assessed whether 
directly manipulating adiposity through lipectomy and fat transplantation 
influences inflammation, cognition, and synaptic plasticity. Lipectomy 
prevents and fat transplantation promotes systemic and central 
inflammation, with associated alterations in cognitive and synaptic 
function. Levels of interleukin 1? (IL1?) emerged as a correlate of 
adiposity and cognitive impairment across both the treadmill and lipectomy 
studies, so we manipulated hippocampal IL1 signaling using 
intrahippocampal delivery of IL1 receptor antagonist (IL1ra). 
Intrahippocampal IL1ra prevented synaptic dysfunction, proinflammatory 
priming, and cognitive impairment. This pattern supports a central role 
for IL1-mediated neuroinflammation as a mechanism for cognitive deficits 
in obesity and diabetes.
KEYWORDS:

diabetes, hippocampus, inflammation, microglia, obesity, synapse

PMID:
     24523551
     [PubMed - in process]
PMCID:
     PMC3921429
     [Available on 2014/8/12]

http://www.ncbi.nlm.nih.gov/pubmed/24523551

.

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Sincerely,
David Dillard
Temple University
(215) 204 - 4584
[log in to unmask]
http://workface.com/e/daviddillard

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Bushell, R. & Sheldon, P. (eds),
Wellness and Tourism: Mind, Body, Spirit,
Place, New York: Cognizant Communication Books.
Wellness Tourism: Bibliographic and Webliographic Essay
David P. Dillard
http://tinyurl.com/p63whl

INDOOR GARDENING
Improve Your Chances for Indoor Gardening Success
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SPORT-MED
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http://listserv.temple.edu/archives/sport-med.html

HEALTH DIET FITNESS RECREATION SPORTS TOURISM
http://health.groups.yahoo.com/group/healthrecsport/
http://listserv.temple.edu/archives/health-recreation-sports-tourism.html






.

.

Please Ignore All Links to JIGLU
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The Net-Gold relationship with JIGLU has
been terminated by JIGLU and these are dead links.
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