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Link between high-fat diet and type 2 diabetes clarified

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Fatty acid--induced NLRP3-ASC inflammasome activation interferes with

insulin signaling*.

Haitao Wen, Denis Gris, Yu Lei, Sushmita Jha, Lu Zhang, Max Tze-Han

Huang, Willie June Brickey, P-Y Ting.

/Nature Immunology/, 2011;

DOI: 10.1038/ni.2022 <http://dx.doi.org/10.1038/ni.2022>

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*/

Link Between High-Fat Diet and Type 2 Diabetes Clarified/*

http://www.sciencedaily.com/releases/2011/04/110411121539.htm

ScienceDaily (Apr. 26, 2011) --- A diet high in saturated fat is a key

contributor to type 2 diabetes, a major health threat worldwide. Several

decades ago scientists noticed that people with type 2 diabetes have

overly active immune responses, leaving their bodies rife with

inflammatory chemicals.

In addition, people who acquire the disease are typically obese and are

resistant to insulin, the hormone that removes sugar from the blood and

stores it as energy.

For years no one has known exactly how the three characteristics are

related. But a handful of studies suggest that they are inextricably linked.

New research from the University of North Carolina at Chapel Hill School

of Medicine adds clarity to the connection. The study published online

April 10 in the journal /Nature Immunology/ finds that saturated fatty

acids but not the unsaturated type can activate immune cells to produce

an inflammatory protein, called interleukin-1beta.

" The cellular path that mediates fatty acid metabolism is also the one

that causes interleukin-1beta production, " says senior study co-author

Y. Ting, PhD, Kenan Rand Professor in the Department of

Microbiology and Immunology.

" Interleukin-1beta then acts on tissues and organs such as the liver,

muscle and fat (adipose) to turn off their response to insulin, making

them insulin resistant. As a result, activation of this pathway by fatty

acid can lead to insulin resistance and type 2 diabetes symptoms. " Ting

is also a member of the UNC Lineberger Comprehensive Cancer Center, and

the UNC Inflammatory Diseases Institute.

Other authors of the report, all in the Department of Microbiology and

Immunology, are postdoctoral researcher and first author Haitao Wen,

Denis Gris, Yu Lei, Shushmita Jha; Lu Zhang, Max Tze-Han Huang, and

Willie June Brickey.

The research was supported in part by the National Institutes of Health

and the American Heart Association Mid-Atlantic Affiliate.

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