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Impaired fat-burning gene worsens diabetes

[PRESSRELEASE 7 February 2008] Researchers at Karolinska Institutet have
in collaboration with researchers from Finland, China, Japan and the US
discovered new cellular mechanisms that lead to in insulin resistance in
people with diabetes. The results are published in the scientific
journal Cell.

Type 2-diabetes is a chronic disease resulting from a reduction in
insulin-production from the pancreas or an inability of other tissues in
the body to respond adequately to the produced insulin, so called
insulin resistance. This leads to increased blood sugar, which in turn
leads to a worsening of the insulin resistance, increasing the risk of
developing many serious diabetes-associated complications.


An international research team, led by Professor Juleen R. Zierath at
Karolinska Institutet have identified previously unknown molecular
mechanisms by which elevated blood sugar leads to impaired insulin
sensitivity in people with diabetes. The research team identified a
'fat-burning' gene, the products of which [Diacylglycerol Kinase Delta]
are required to maintain the cells insulin sensitivity. They also
discovered that this gene is reduced in muscle tissue from people with
high blood sugar and type 2-diabetes. In the absence of the enzyme
[Diacylglycerol Kinase Delta] that is made by this gene, muscles have
reduced insulin sensitivity, impaired fat burning ability, which leads
to an increased risk of developing obesity.

"The expression of this gene is reduced when blood sugar rises, but
activity can be restored if blood sugar is controlled by pharmacological
treatment or exercise", says Professor Juleen Zierath. "Our results
underscore the importance of tight regulation of blood sugar for people
with diabetes."

Publication:


Down-Regulation of Diacylglycerol Kinase Delta Contributes to
Hyperglycemia-Induced Insulin Resistance

Cell, 8 februari 2008, online 7 februari 2008

Alexander V. Chibalin, Ying Leng, Elaine Vieira, Anna Krook, Marie
Björnholm, Yun Chau Long, Olga Kotova, Zhihui Zhong, Fumio Sakane,
Tatiana Steiler, Carolina Nylén, Jianjun Wang, Markku Laakso, Matthew K.
Topham, Marc Gilbert, Harriet Wallberg-Henriksson och Juleen R. Zierath

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