[acb-diabetics] FW: [blind-diabetics] Fw: [BDA] Article:

Tue Jun 28 13:45:35 EDT 2011

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From: blind-diabetics at yahoogroups.com
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Sent: Tuesday, June 28, 2011 8:33 AM
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Subject: [blind-diabetics] Fw: [BDA] Article:

It's not an apple a day after all -- it's strawberries: Flavonoids could
represent two-fisted assault on diabetes and nervous system disorders

A recent study from scientists at the Salk Institute for Biological Studies
suggests that a strawberry a day (or more accurately, 37 of them) could keep
not just one doctor away, but an entire fleet of them, including the
neurologist, the endocrinologist, and maybe even the oncologist. 
See Also: 
Investigations conducted in the Salk Institute's Cellular Neurobiology
Laboratory (CNL) will appear in the June 27, 2011, issue of PLoS ONE. The
report explains that fisetin, a naturally-occurring flavonoid found most
abundantly in strawberries and to a lesser extent in other fruits and
vegetables, lessens complications of diabetes. Previously, the lab showed
that fisetin promoted survival of neurons grown in culture and enhanced
memory in healthy mice. That fisetin can target multiple organs strongly
suggests that a single drug could be used to mitigate numerous medical
complications. 
"This manuscript describes for the first time a drug that prevents both
kidney and brain complications in a type 1 diabetes mouse model," says David
Schubert, Ph.D., professor and head of the Cellular Neurobiology Laboratory
and one of the manuscript's co-authors. "Moreover, it demonstrates the
probable molecular basis of how the therapeutic is working." 
Pam Maher, Ph.D., a senior staff scientist in the CNL, is the study's
corresponding author. Maher initially identified fisetin as a
neuroprotective flavonoid ten years ago. "In plants, flavonoids act as
sunscreens and protect leaves and fruit from insects," she explains. "As
foods they are implicated in the protective effect of the 'Mediterranean
Diet.'" 
Other celebrity flavonoids include polyphenolic compounds in blueberries and
red wine. 
Although her group's focus is neurobiology, Maher and colleagues reasoned
that, like other flavonoids, fisetin might ameliorate a spectrum of
disorders seen in diabetic patients. To test this, they evaluated effects of
fisetin supplementation in Akita mice, a very robust model of type 1
diabetes, also called childhood onset diabetes. 
Akita mice exhibit increased blood sugar typical of type 1 diabetes and
display pathologies seen in serious human complications of both type 1 and 2
diabetes. Those include diabetic nephropathy or kidney disease, retinopathy,
and neuropathies in which patients lose touch or heat sensations. 
Mice fed a fisetin-enriched diet remained diabetic, but acute kidney
enlargement-or hypertrophy-seen in untreated mice was reversed, and high
urine protein levels, a sure sign of kidney disease, fell. Moreover, fisetin
ingestion ameliorated anxiety-related behaviors seen in diabetic mice. "Most
mice put in a large area become exploratory," says Maher. "But anxious mice
tend not to move around. Akita mice showed enhanced anxiety behavior, but
fisetin feeding restored their locomotion to more normal levels." 
The study also defines a likely molecular mechanism underlying these
effects. Researchers observed that blood and brain levels of sugars affixed
to proteins known as advanced glycation end-products-or AGEs-were reduced in
fisetin-treated compared to untreated Akita mice. These decreases were
accompanied by increased activity of the enzyme glyoxalase 1, which promotes
removal of toxic AGE precursors. 
The discovery of an AGE-antagonizing enzyme upregulated by fisetin is very
intriguing, because substantial evidence implicates high blood AGE levels
with many if not most diabetic complications. "We know that fisetin
increases activity of the glyoxalase enzyme and may increase its
expression," says Maher. "But what is important is that ours is the first
report that any compound can enhance glyoxalase 1 activity." 
Interestingly, excessively high AGE levels also correlate with inflammatory
activity thought to promote some cancers. In fact, studies published by
others confirm that fisetin decreases tumorigenicity of prostate cancer
cells both in culture and in animal models, which if supported would
represent a major added incentive to eat your strawberries. 
To ingest fisetin levels equivalent to those fed Akita mice, Maher estimates
that humans would have to eat 37 strawberries a day, assuming that
strawberry fisetin is as readily metabolizable by humans as fisetin-spiked
lab chow is by mice. Rather than through diet, Maher envisions that
fisetin-like drugs could be taken as a supplement. 
Schubert notes that fisetin is also effective in mouse models of Alzheimer's
disease. "We and others have shown that diabetes may be a risk factor for
Alzheimer's disease, making identification of a safe prophylactic like
fisetin highly significant," he says. 
Maher acknowledges that the public may be suffering from flavonoid-fatigue,
given media coverage of the promises of these compounds. "Polyphenolics like
fisetin and those in blueberry extracts are found in fruits and vegetables
and are related to each other chemically," she says. "There is increasing
evidence that they all work in multiple diseases. Hopefully some combination
of these compounds will eventually get to the clinic." 
Schubert concurs that their findings only reinforce what common sense and
our mothers told us was a healthy lifestyle. "Eat a balanced diet and as
much freshly prepared organic food as possible, get some exercise, keep
socially and mentally active and avoid sodas with sugar and highly processed
foods since they can contain high levels of AGEs," he advises. 
But he also worries that hoops that must be jumped through to bring a
natural product like fisetin, as opposed to a totally synthetic drug, to
clinical trials are daunting because it is difficult to protect patents on
natural products. "We will never know if a compound like fisetin works in
humans until someone is willing to support a clinical trial." 
Also contributing to this study were Richard Dargusch and Jennifer L. Ehren,
Ph.D.,of the Cellular Neurobiology Laboratory, and Kumar Sharma, M.D., and
Shinichi Okada, M.D., Ph.D., of the Department of Medicine at University of
California, San Diego. 
Funding for the study came from the Fritz B. Burns Foundation, the Juvenile
Diabetes Research Foundation, the Hewitt Foundation, and the National
Institutes of Health. 

[Non-text portions of this message have been removed]

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