New Enzyme Blocks Pancreatic Insulin Production
Linda von Wartburg
2 December 2007

Scientists from Sydney, Australia, recently identified and mapped the
structure of an enzyme that cuts down insulin production in diabetes.
Called protein kinase C epsilon (PKCe), it is regulated by fat. For
that reason, it may be the missing link that relates obesity to type 2
diabetes.

The researchers, based in Sydney, Australia, genetically engineered
some mice so that they didn't have any PKCe. Even after the mice were
fattened up with a high fat diet that would otherwise have made them
diabetic, they didn't develop type 2 diabetes. They did become insulin
resistant, but their insulin production, uninhibited by PKCe, kept
rolling along nicely.

The researchers believe that by blocking the action of PKCe, they
might be able to restore the pancreas's insulin production back to
normal. A drug that inhibited PKCe could result in greater insulin
production by the pancreas only when it was needed, such as when
glucose levels rise after a meal. As such, it would be a big
improvement over the current {*filter*} that force the beta cells to pump
out more insulin willy-nilly, no matter what the circumstances. Such a
drug, however, is a rather distant dream at the moment, probably ten
years off (as usual).

Sources: Cell Metabolism, October 2007; ScienceAlert; Bloomberg.com

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"more short fatty acids than longer chains"
"free from insulin resistance and diabetes"

Not all fat harms liver
Wednesday, 03 October 2007 Tan Ee Lyn

Reuters

While it has long been held that too much fat in the liver may result
in diabetes, researchers appear to have discovered that not all types
of fat are harmful.

Writing in the latest issue of the journal Nature Medicine, a group
of
Japanese scientists describe how they changed the fat composition in
the livers of mutant mice and fed them exactly the same rich, fatty
diet as other mice.

All the rodents became obese and the normal mice developed resistance
to insulin, then became prone to diabetes. But the mutant mice were
free from those problems.

"Obesity is a matter of quantity of fats in the body. But it is our
new message that the quality of fats could be a new determinant
factor for diabetes," says Associate Professor Hitoshi Shimano of the
Graduate School of Comprehensive Human Sciences at the University of
Tsukuba.

Excessive fat intake leads to obesity and overwhelms the storage
capacity of fat cells, with surplus fat stored in the liver.

Development of fatty liver can result in insulin resistance and
increased glucose levels, hallmarks of diabetes.

"The absolute levels of fat in the liver do not therefore seem to be
detrimental to maintaining normal glucose levels. Instead, the types
of fat that are present seem to be a more important factor, with
shorter fat molecules being healthier than longer ones," the
researchers write.

Obese but not diabetic

Shimano and his colleagues created a batch of mice lacking Elovl6, an
enzyme that increases the length of the carbon chains of fatty acids.

That changed the fat composition in the liver of these mutant, or
knock-out (KO) mice, which ended up with more short fatty acids than
longer chains.

"Unlike normal mice that became insulin resistant and prone to
diabetes after they became obese, the KO mice were free from insulin
resistance and diabetes. In other words, we made mice that did not
become diabetic even after they became obese."

Shimano hopes that {*filter*} can be made to inhibit this enzyme in people
and change the fat composition in their livers so that the risk of
diabetes could be reduced for those who are obese and who find it
hard to lose weight.

"If what we found in these mice is applicable to humans, a drug that
inhibits this enzyme could be a miracle anti-diabetic drug that does
not require diet," Shimano write.

Who loves ya.
Tom

Jesus Was A Vegetarian!
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Man Is A Herbivore!
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DEAD PEOPLE WALKING
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