Researchers find Diabetes trigger, implications in heart disease

From: Sharon Hope (shope_at_anet.net)
Date: 02/03/05 

Date: Wed, 2 Feb 2005 20:58:22 -0800

A friend brought this article to my attention. The breakthrough that was
made has implications for heart disease as well as for Diabetes.

A little bit of an editorial, my response to my friend (after thanking him):

Sharon A. Hope wrote:
> Wow. I had read elsewhere that fat, commonly thought of as inert
> blubber previously, actually becomes its own endocrine system and takes
> actions similar to other glands.
>
> The interesting thing, too, is that they are still into treating a
> symptom.
>
> In other words, the inflammation is a body's immune system response to
> some irritant. Since they don't understand the irritant, they are
> attacking the body's immune response instead, short-cutting it.
>
> Note the reference to heart disease: "Nonetheless, researchers at Joslin
> were excited about their findings and are preparing federal grant
> requests to fund a major, multicity trial of salicylate therapy for type
> 2 diabetes. And there are indications that the drugs could also help
> stave off heart disease."
>
> Why is it that there is never a mention of finding out what it is that
> the body is protecting itself against, and taking care of that? Oh,
> yeah, then you couldn't sell the maintenance drug for life.
>
> Right now, cancer is the one big problem (well, cancer and AIDS), that
> switches
> off the immune system reaction and then takes advantage of that guard
> being down. Why is the current conventional wisdom to make the body
> more clueless, like it is in respect to cancer? Vs saying, OK there is
> something bad going on here, the body is fighting it, but needs help,
> how do we help the body stamp out whatever that bad thing is? No, they
> want to disable the defense instead.
>
> I know, lighten up.
>

To which my wise friend noted:

Sharon, as far as "root cause treatment", it's already common knowledge
that death by starvation cures the underlying problem.

Here is the article:

http://www.boston.com/news/globe/health_science/articles/2005/01/31/researchers_find_diabetes_trigger_possible_fix?mode=PF
Researchers find diabetes trigger, possible fix
By Raja Mishra, Globe Staff | January 31, 2005

Researchers in Boston have pinpointed a primary trigger for the most common
form of diabetes and have uncovered evidence that simple, inexpensive
aspirin-like drugs could keep the disease that affects millions in check.

The researchers, from Joslin Diabetes Center in Boston, discovered a genetic
''master switch" in the liver that is turned on when people become obese.
Obesity has long been linked to diabetes, but the reason, until now, has
been unknown. Joslin researchers found that once on, this switch produces
low-level inflammation, which disrupts the body's ability to process
insulin, causing type 2 diabetes.

But the researchers took the finding one step further. Reasoning that
aspirin-like drugs are used to quell inflammation, they successfully used
the drugs, called salicylates, to eliminate the symptoms of type 2 diabetes
in mice. Human tests are already underway in Boston, though no results have
been published.

''These drugs, among the safest drugs known, can do a surprisingly good job
of toning down this inflammation," said Joslin researcher Dr. Steven E.
Shoelson, lead author of the paper. ''These are hopeful ideas for the
future."

Shoelson warned against rushing out to get salicylates. Their effectiveness
has been proved thus far only in mice.

''No one should go out and take these drugs," said Shoelson. He said losing
weight, exercising, and eating healthy are the obvious things to do.

Nonetheless, researchers at Joslin were excited about their findings and are
preparing federal grant requests to fund a major, multicity trial of
salicylate therapy for type 2 diabetes. And there are indications that the
drugs could also help stave off heart disease.

''There is good reason to believe that this could develop into a therapy for
diabetes. The evidence is quite good," said Dr. Gokhan Hotamisligil,
professor of genetics and metabolism at Harvard School of Public Health, who
was not involved in the study. ''I'm fully convinced this is where the key
therapies for diabetes will emerge from."

The findings appeared yesterday in the online version of the journal Nature
Medicine. The work was funded by the federal government and the American
Diabetes Association.

About 18 million Americans have diabetes, and most have type 2 diabetes. In
type 2 diabetes, the body's cells become resistant to insulin, which
transports sugar from the bloodstream into cells, giving cells energy to
function. In diabetes, this feeding is blocked, causing sugar to build up in
blood.

Those afflicted grow excessively thirsty, exhausted, and confused if the
condition goes untreated, and are at high risk for heart disease, stroke,
blindness, and amputations. About three-quarters of sufferers are obese or
overweight.

Shoelson's team began the experiment seeking the biological connections
between weight gain and diabetes. They knew that the livers of obese people
accumulate fat faster than any other organ, and that many overweight
diabetic patients had high levels of proteins -- particularly one called
NF-kB -- in their livers that normally trigger inflammation.

They zeroed in on it and were stunned to discover its role in diabetes. The
scientists were able to trigger inflammation and the symptoms of diabetes in
lean, previously healthy mice by using genetic techniques to turn on the
gene that makes NF-kB.

Normally, in response to an infection, the liver produces massive amounts of
NF-kB, which triggers a biological process that sends white blood cells to
an injury site to fight off infections, causing inflammation in the process.
NF-kB acts as a master switch, triggering this complex and life-saving
reaction.

But in obese mice, Shoelson's team found that a fatty liver -- for reasons
still unknown -- also flipped on NF-kB, though at far lower levels. The
proteins secreted when this low-level inflammation occurs disrupt the body's
ability to process insulin, leading to diabetes.

''We previously knew that in obesity, the liver becomes fatty and that it
accumulates fat faster than other organs and tissues," said Shoelson. ''But
until now, we didn't know fat in the liver could orchestrate the entire
inflammatory process that results in insulin resistance, both locally and
throughout the body."

Shoelson's team decided to use salicylates, already used as
anti-inflammatories, to try to stop low-level inflammation and diabetes
symptoms triggered by NF-kB -- and was successful. As long as the mice got
adequate doses, their diabetes was held in check. Aspirin is the best known
of this family of drugs. But Shoelson found that it would take more than 20
aspirins daily to suppress NF-kB in human diabetics, which would cause
severe gastrointestinal bleeding.

In human trials, Shoelson is using a milder, commercially available
prescription salicylate called salsalate, used safely by thousands to treat
joint pain. He is negotiating with the National Institutes of Health to fund
a large-scale national trial.

Another intriguing finding emerged from the study: Within the complex
cascade of biological events triggered by NF-kB, Shoelson found that
C-reactive protein levels were elevated. C-reactive protein, or CRP, has
been found to be a strong risk marker for heart disease.

Shoelson is preparing an experiment to test if salicylates also can reduce
CRP and thus heart disease risk.

Raja Mishra can be reached at rmishra@globe.com.

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