Re: [IP] Surgery for Type 2 Diabetes.
John Wilkinson wrote:
International Conference on Gastrointestinal Surgery to Treat Type 2
Recent studies demonstrate that some bariatric operations and
procedures can ameliorate diabetes. Consequently, these operations
are being used throughout the world to treat diabetes in association
with obesity, and increasingly, for diabetes alone.
Stacey and Kathleen, you both may be interested in a recent study
regarding fat loss.
Researchers at Penn State think they have isolated the enzyme that
stops the synthesis of fat in the body. The interesting thing is they
were able to trigger a starvation response in mice. By depriving the
mice of leucine (an amino acid), they were able to stop the mice from
synthesizing new fat cells and start drawing from their current fat
stores. No drug involved in their treatment, only the minimization
of leucine intake.
The findings are also applicable to those who fail to gain weight
despite sufficient calorie intake. It appears that calories alone are
not sufficient for weight gain if leucine levels are low.
I don't know if the treatment is ready for prime time, but quoting
"These findings are important for treating two major problems in the
world," Cavener said. "The starvation response we discovered can
repress fat synthesis and induce the body to consume virtually all of
its stored fat within a few weeks of leucine deprivation. Because
this response causes a striking loss of fatty tissue, we may be able
to formulate a powerful new treatment for obesity".
Trick the Body into Starving on a Plentiful Diet?
Researchers from Penn State, published in the February 7, 2007 Cell
Metabolism, have discovered that when mice are deprived of only a
single amino acid, their metabolisms are fooled into thinking they
are starving. In response, they stop synthesizing new fats and they
use up all their fat stores, losing 97 percent of their body fat in
The researchers found that a certain enzyme, called GCN2 eIF2a
kinase, is the critical player that kicks the body into starvation
mode. It does this by monitoring deficiencies in amino acids. Removal
of just a single amino acid, leucine, from the diet of the mice was
sufficient to trigger GCN2 to start a starvation response. Despite
the fact that the mice were consuming normal amounts of carbohydrates
and fats, they shut down fat synthesis in the liver and mobilized
their stored fat deposits. Their bodies were literally tricked into
starvation mode by the fact that leucine was missing from the diet.
After 17 days of a leucine-deficient diet, the mice lost 48 percent
of their liver mass and 97 percent of the adipose or fatty tissue
from their abdomens. The response was very similar to what happens
during starvation. In contrast, control mice bred to be missing the
GCN2 kinase enzyme kept a steady liver mass and lost only 69 percent
of the adipose tissue on their abdomens
Dx'd 1967, Pumping since 1/14/2004 w/ Animas IR1000, 7/2/2004 -
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