[acb-diabetics] reason for blood vessel damage in diabetics

Sat Feb 5 23:25:26 GMT 2011

Cause of Blood Vessel Damage in People with Diabetes Discovered

Researchers have identified a key mechanism that appears to contribute to
blood vessel damage in people with diabetes....

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The researchers said studies in mice show that the damage appears to involve
two enzymes, fatty acid syntheses (FAS) and nitric oxide syntheses (NOS)
that interact in the cells that line blood vessel walls. First author
Xiaochao Wei said, "We already knew that in diabetes there's a defect in the
endothelial cells that line the blood vessels."  

"People with diabetes also have depressed levels of fatty acid synthase. But
this is the first time we've been able to link those observations together."

Wei studied mice that had been genetically engineered to make FAS in all of
their tissues except the endothelial cells that line blood vessels. These
so-called FASTie mice experienced problems in the vessels that were similar
to those seen in animals with diabetes. "It turns out that there are strong
parallels between the complete absence of FAS and the deficiencies in FAS
induced by lack of insulin and by insulin resistance," said Clay F.
Semenkovich, the Herbert S. Gasser Professor of Medicine, professor of cell
biology and physiology and chief of the Division of Endocrinology,
Metabolism and Lipid Research, Washington University in St. Louis, Missouri.

Comparing FASTie mice to normal animals, as well as to mice with diabetes,
Wei and Semenkovich determined that mice without FAS, and with low levels of
FAS, could not make the substance that anchors nitric oxide synthase to the
endothelial cells in blood vessels. "We've known for many years that to have
an effect, NOS has to be anchored to the wall of the vessel," Semenkovich
said.  

"Xiaochao discovered that fatty acid synthase preferentially makes a lipid
that attaches to NOS, allowing it to hook to the cell membrane and to
produce normal, healthy blood vessels." In the FASTie mice, blood vessels
were leaky, and in cases when the vessel was injured, the mice were unable
to generate new blood vessel growth. 

The actual mechanism involved in binding NOS to the endothelial cells is
called palmitoylation. Without FAS, the genetically engineered mice lose NOS
palmitoylation and are unable to modify NOS so that it will interact with
the endothelial cell membrane. That results in blood vessel problems.   

It's a long way, however, from a mouse to a person, so the researchers next
looked at human endothelial cells, and they found that a similar mechanism
was at work.

"Our findings strongly suggest that if we can use a drug or another enzyme
to promote fatty acid synthase activity, specifically in blood vessels, it
might be helpful to patients with diabetes," Wei said.

Journal of Biological Chemistry. Jan. 2011

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This article originally posted 01 February, 2011 and appeared in
Complications and Co-morbidities
<http://www.diabetesincontrol.com/topics/complications-and-co-morbidities> ,
Issue 559
<http://www.diabetesincontrol.com/diabetes-in-control-newsletters/559>  

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