http://www.sciencedaily.com/releases/2008/03/080305113659.htm

When the upper gut is bypassed there is a large increase in the incretin
glp-1 which is found in higher levels from the l cells of the lower
smallgut and large gut.  Glp-1 works like the drug byetta which prompts
insulin release when glucose levels rise.

Large increases in glp-1 have been measured in bypass patients because
food whichprompts glp-1 production has not been largely digested as it
would have been in the upper gut but thrown instead into the area of
densest glp-1 production.  In a very few there is so much that it
produces an insulin created hypo situation.

Also in the upper gut and decreasing along its length and largely absent
in the large gut are d cells which produce somatastatin which is
acounterregulatory hormone for glp-1.  Thus in a bypass patient the area
of the most somatastatin production In the upper gut is also missing.

It seems to me the process the person in the article suggests be found
has in fact already been known and described.

http://www.sciencedaily.com/releases/2008/03/080305113659.htm

When the upper gut is bypassed there is a large increase in the incretin
glp-1 which is found in higher levels from the l cells of the lower
smallgut and large gut.  Glp-1 works like the drug byetta which prompts
insulin release when glucose levels rise.

Large increases in glp-1 have been measured in bypass patients because
food whichprompts glp-1 production has not been largely digested as it
would have been in the upper gut but thrown instead into the area of
densest glp-1 production.  In a very few there is so much that it
produces an insulin created hypo situation.

Also in the upper gut and decreasing along its length and largely absent
in the large gut are d cells which produce somatastatin which is
acounterregulatory hormone for glp-1.  Thus in a bypass patient the area
of the most somatastatin production In the upper gut is also missing.

It seems to me the process the person in the article suggests be found
has in fact already been known and described.

From your cite:

ScienceDaily (Mar. 5, 2008) -- Growing evidence shows that surgery may
effectively cure Type 2 diabetes -- an approach that not only may
change the way the disease is treated, but that introduces a new way
of thinking about diabetes.

A new article -- published in a special supplement to the February
issue of Diabetes Care by a leading expert in the emerging field of
diabetes surgery -- points to the small bowel as the possible site of
critical mechanisms for the development of diabetes.

The study's author, Dr. Francesco Rubino of NewYork-Presbyterian
Hospital/Weill Cornell Medical Center, presents scientific evidence on
the mechanisms of diabetes control after surgery. Clinical studies
have shown that procedures that simply restrict the stomach's size
(i.e., gastric banding) improve diabetes only by inducing massive
weight loss. By studying diabetes in animals, Dr. Rubino was the first
to provide scientific evidence that gastrointestinal bypass operations
involving rerouting the gastrointestinal tract (i.e., gastric bypass)
can cause diabetes remission independently of any weight loss, and
even in subjects that are not obese.

"By answering the question of how diabetes surgery works, we may be
answering the question of how diabetes itself works," says Dr. Rubino,
who is a professor in the Department of Surgery at Weill Cornell
Medical College and chief of gastrointestinal metabolic surgery at
NewYork-Presbyterian/Weill Cornell.

Dr. Rubino's prior research has shown that the primary mechanisms by
which gastrointestinal bypass procedures control diabetes specifically
rely on the bypass of the upper small intestine -- the duodenum and
jejunum. This is a key finding that may point to the origins of
diabetes.

"When we bypass the duodenum and jejunum, we are bypassing what may be
the source of the problem," says Dr. Rubino, who is heading up NewYork-
Presbyterian/Weill Cornell's Diabetes Surgery Center.

In fact, it has become increasingly evident that the gastrointestinal
tract plays an important role in energy regulation, and that many gut
hormones are involved in the regulation of sugar metabolism. "It
should not surprise anyone that surgically altering the bowel's
anatomy affects the mechanisms that regulate blood sugar levels,
eventually influencing diabetes," Dr. Rubino says.

While other gastrointestinal operations may cure diabetes as an effect
of changes that improve blood sugar levels, Dr. Rubino's research
findings in animals show that procedures based on a bypass of the
upper intestine may work instead by reversing abnormalities of blood
glucose regulation.

In fact, bypass of the upper small intestine does not improve the
ability of the body to regulate blood sugar levels. "When performed in
subjects who are not diabetic, the bypass of the upper intestine may
even impair the mechanisms that regulate blood levels of glucose,"
says Dr. Rubino. In striking contrast, when nutrients' passage is
diverted from the upper intestine of diabetic patients, diabetes
resolves.

This, he explains, implies that the upper intestine of diabetic
patients may be the site where an abnormal signal is produced,
causing, or at least favoring, the development of the disease.

How exactly the upper intestine is dysfunctional remains to be seen.
Dr. Rubino proposes an original explanation known in the scientific
community as the "anti-incretin theory."

Incretins are gastrointestinal hormones, produced in response to the
transit of nutrients, that boost insulin production. Because an excess
of insulin can determine hypoglycemia (extremely low levels of blood
sugar) -- a life-threatening condition -- Dr. Rubino speculates that the
body has a counter-regulatory mechanism (or "anti-incretin"
mechanism), activated by the same passage of nutrients through the
upper intestine. The latter mechanism would act to decrease both the
secretion and the action of insulin.

"In healthy patients, a correct balance between incretin and anti-
incretin factors maintains normal excursions of sugar levels in the
bloodstream," he explains. "In some individuals, the duodenum and
jejunum may be producing too much of this anti-incretin, thereby
reducing insulin secretion and blocking the action of insulin,
ultimately resulting in Type 2 diabetes."

Indeed, in Type 2 diabetes, cells are resistant to the action of
insulin ("insulin resistance"), while the pancreas is unable to
produce enough insulin to overcome the resistance.

After gastrointestinal bypass procedures, the exclusion of the upper
small intestine from the transit of nutrients may offset the abnormal
production of anti-incretin, thereby resulting in remission of
diabetes.

In order to better understand these mechanisms, and help make the
potential benefits of diabetes surgery more widely available, Dr.
Rubino calls for prioritizing research in diabetes surgery. "Further
research on the exact molecular mechanisms of diabetes, surgical
control of diabetes and the role played by the bowel in the disease
may bring us closer to the cause of diabetes."

Today, most patients with diabetes are not offered a surgical option,
and bariatric surgery is recommended only for those with severe
obesity (a body mass index, or BMI, of greater than 35kg).

"It has become clear, however, that BMI cut-offs can no longer be used
to determine who is an ideal candidate for surgical treatment of
diabetes," says Dr. Rubino.

"There is, in fact, growing evidence that diabetes surgery can be
effective even for patients who are only slightly obese or just
overweight. Clinical trials in this field are therefore a priority as
they allow us to compare diabetes surgery to other treatment options
in the attempt to understand when the benefits of surgery outweigh its
risks. Clinical guidelines for diabetes surgery will certainly be
different from those for bariatric surgery, and should not be based
only on BMI levels," he notes.

"The lesson we have learned with diabetes surgery is that diabetes is
not always a chronic and relentless disease, where the only possible
treatment goal is just the control of hyperglycemia and minimization
of the risk of complications. Gastrointestinal surgery offers the
possibility of complete disease remission. This is a major shift in
the way we consider treatment goals for diabetes. It is unprecedented
in the history of the disease," adds Dr. Rubino.

Type 2 diabetes, which accounts for 90 to 95 percent of all cases of
diabetes, is a growing epidemic that afflicts more than 200 million
people worldwide.

At a time when diabetes is growing epidemically worldwide, Dr. Rubino
says that finding new treatment strategies is a race against time. "At
this point, missing the opportunity that surgery offers is not an
option."

In addition to having performed landmark studies in the field of
diabetes surgery, Dr. Rubino was the principal organizer of an
influential Diabetes Surgery Summit, held in Rome in March 2007. This
international consensus conference helped establish the field, making
international recommendations for the use of surgery and creating an
International Diabetes Surgery Task Force. Dr. Rubino serves as a
founding member.

*** end article ***

It remains much smarter to willfully choose to eat less, down to the
right amount ...

http://HeartMDPhD.com/BeSmart

... to lose all the black fat, which is the real cause of the insulin
resistance (IR/MetS) that undergirds type-2 diabetes:

http://HeartMDPhD.com/OffalFat

http://HeartMDPhD.com/BlackFat

Farm animals do start dropping dead after they have been fattened to
the point of acquiring black fat.

Be hungry... be healthy... be hungrier... be euglycemic:

http://TheWellnesFoundation.com/BeHealthy

Prayerfully in the infinite power and might of the Holy Spirit,

Andrew <><
--
Andrew B. Chung, MD/PhD
Lawful steward of http://EmoryCardiology.com
Brethren of the KING of kings and LORD of lords.
http://HeartMDPhD.com/ChristianBrethren

More is said in the Science Daily release than in the following
abstract.  I often keep a copy of an abstract in a pending file
as a reminder to access the full article when it is available.
Since this was published in the February 2008 issue the full article
should be available in August (6 months).

Is Type 2 Diabetes an Operable Intestinal Disease? -
http://tinyurl.com/3bgmnk or
http://care.diabetesjournals.org/cgi/content/abstract/31/Supplement_2/S290

This is peculiar in that the duodenum is where the duct from the
exocrine pancreas secretes the enzyme that breaksdown fats,
carbohydrates, and proteins. The duodenum is also the location of the
duct that secretes the concentrated bile from the gall bladder that is
initially produced in the liver. The jejunum is the location of the
K-type cells that produce the incretin hormone GIP. All indications are
that this was an animal study.  At this point the bypass does not make
sense to me. ;)

"Dr. Rubino's prior research has shown that the primary mechanisms by
which gastrointestinal bypass procedures control diabetes specifically
rely on the bypass of the upper small intestine -- the duodenum and
jejunum. This is a key finding that may point to the origins of
diabetes.

"When we bypass the duodenum and jejunum, we are bypassing what may be
the source of the problem," says Dr. Rubino, who is heading up NewYork-
Presbyterian/Weill Cornell's Diabetes Surgery Center.

In fact, it has become increasingly evident that the gastrointestinal
tract plays an important role in energy regulation, and that many gut
hormones are involved in the regulation of sugar metabolism. "It
should not surprise anyone that surgically altering the bowel's
anatomy affects the mechanisms that regulate blood sugar levels,
eventually influencing diabetes," Dr. Rubino says.

While other gastrointestinal operations may cure diabetes as an effect
of changes that improve blood sugar levels, Dr. Rubino's research
findings in animals show that procedures based on a bypass of the
upper intestine may work instead by reversing abnormalities of blood
glucose regulation."