[acb-diabetics] changes in fat cells...

[Patricia LaFrance-Wolf]

his article originally posted 16 July, 2010 and appeared in  

Issue 530

 

Changes in Fat Cells May Pave Way for Type 2 Diabetes

 

Cellular changes in fat tissue play a major role in the development of Type
2 diabetes and may result in the "hyperinflammation" a new study shows.... 

 

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University of Cincinnati researchers found that these changes in fat cells
-- not the immune system, as previously thought -- are linked to the
"hyperinflammation"

seen in obesity-related glucose intolerance and Type 2 diabetes. The
findings, they said, may eventually lead to the development of new drugs to
treat

Type 2 diabetes and may also offer insights into the formation of aggressive
cancers.

 

Jorge Moscat, the study's principal investigator and chair of UC's cancer
and cell biology department, in a university news release, stated that,
"This

finding is quite novel because current drug development efforts target
immune cells (macrophages, T-cells) to eliminate this hyperinflammation....
Our

research suggests obesity-related glucose intolerance has nothing to do with
the immune system. It may be more effective to target (fat cells)."

 

In laboratory animals, the researchers found that a gene known as protein
kinase C (PKC)-zeta plays a dual role in molecular signaling associated with
inflammation.

Obesity, they said, can switch the gene from acting as an inflammation
regulator to an agent promoting inflammation. PKC-zeta does this by causing
fat

cells to secrete a substance called interleukin-6 (IL6), which streams to
the liver in large quantities to cause insulin resistance.

 

Previous research has linked PKC-zeta to the development of malignant
tumors. Researchers say it may do so in a manner similar to the way in which
it triggers

the inflammation associated with diabetes.

 

"Now we are trying to understand how PKC-zeta regulates IL6 to better
determine how we can manipulate the protein to help prevent diabetes and
cancer,"

Moscat said.

 

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