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Old November 16th, 2005, 04:10 PM
John G.
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Default Ketogenic Diet Raises Brain Energy (Press Release)

Given the clear benefits of a ketogenic diet, fat-busting per se is
probably short-sighted. Nevertheless, here are some notes on
CD36. I wonder how much in the way of ketogenic benefits
stem from some sort of CD36 action.

CD36 null mice have much less fatty acid uptake in heart,
skeletal muscle and adipose tissues and less incorporation of
fatty acids into triglycerides leading to an accumulation of
diaglycerides; CD36 is heavily expressed in these organs
[PMID 11478366]

human cells recognize foreign antigens via the TLR system;
CD36 scavenges potentially dangerous endogenous molecules
from the body like oxidized and crosslinked proteins; CD36
may be a mediator in sterile inflammation and the TLR system
may be involved as well; some TLR2 ligands related to
bacterial infection are dependent on CD36
http://www.sciencedaily.com/releases/2005/03/050326002258/htm,
[PMID 15690042]

pregnant mice on a low-carb, high-fat diet ate fewer calories and
had offspring which with half the liver triglycerides and higher
levels of hepatic proteins like CD36, CPT-1 and PPARalpha
http://www.sciencedaily.com/releases/2004/11/041123111459.htm

a high unsaturated fat, high protein, low carbohydrate diet for
pregnant rats dramatically lowered hepatic triglycerides and
raised PPARalpha, CD36 and carnitine palmitoyltransferase-1
(CPT-1) in their adult female offspring [PMID 15319218]
(hyperglycemia triggers overexpression of CD36 in kidney cells
leading to chronic kidney disease after substances in diabetic
blood bind to CD36 and trigger the death of these kidney cells
http://www.sciencedaily.com/releases/2005/02/050223125732.htm);

green tea catechins downregulate genes for PPARgamma, CD36,
LXR-alpha, C-myc and upregulates transcription of PPARalpha
and LDL-R (LDL receptor); this may be how green tea inhibits
atherosclerosis [PMID 15022174]

http://www.scientificamerican.com/ar...&articleID=000

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November 14, 2005 Newsletters | RSS
SCIENCE NEWS

Potential Taste Receptor for Fat Identified

French scientists have identified a protein receptor that resides
in the taste buds and may be responsible for sensing fat. As such,
this so-called fatty acid transporter, known as CD36, could be to
blame for our love of high-fat foods--and could thus serve as a
possible target for treatment of obesity.

If the link bears out, CD36 would allow fat to join the five previously
identified tastes that govern the experience of food: bitter, salty,
sweet, sour and "umami," or savoriness (like the meaty goodness
of soup stock).

Researchers have long debated whether a sensor for fat existed,
given that many animals display an innate attraction to fats. To
determine whether CD36 -- a protein expressed in the taste
buds -- might be the culprit, a team at the University of Bourgogne
devised an experiment using mice that had been genetically
modified to lack CD36. These mice, along with a group of wild
mice were fed two solutions: one laced with fat and one containing
xanthan gum to mimic fat's mouthfeel.

Wild mice craved the fatty solution. The mice missing CD36, in
contrast, showed no preference either way. In addition, neither
group exhibited a change in either their desire for sugar or aversion
to quinine, indicating that CD36's effect was limited to fats.

Furthermore, removal of the CD36 gene in rats prevented their
digestive tracts from preparing the various gastric juices necessary
to digest fat. "Because expression of CD36 within the oral cavity
and its effect on digestive secretions are conserved in mice and
rats, it is likely that CD36 performs a basic function in the taste
bud cells," Philippe Besnard and his fellow authors conclude in
the current issue of the Journal of Clinical Investigation.

The authors caution, however, that further studies are needed to
determine whether CD36 is indeed the elusive fat sensor, how it
signals fat to the taste bud, and, ultimately, why that prompts
craving. "The sensory experience of food can be a primary
reinforcer of intake," writes Nada Abumrad of Washington
University in an accompanying commentary. "As more is learned
about the specificity and mechanism of this receptor's function,
it may be possible to devise strategies to treat some forms of
obesity." --David Biello