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Unusual suspect: Hopkins scientists find 'second fiddle' protein's role in Type 2 diabetes
Date:4/11/2013

ne-secreting pancreatic cells known as islets of Langerhans to keep up with the body's demand for insulin. Insulin regulates blood sugar by transporting glucose from the blood into organs and tissues for fuel or storage. The body normally releases extra insulin when blood sugar levels surge after eating, but repeated or continued overeating and high-fat diets put added demand on the pancreas to churn out more insulin to keep up with constantly high blood sugar levels. The chronically overworked beta cells eventually slow down their insulin output until it ceases altogether. Insulin deficiency causes abnormal buildup of glucose in the blood and the body's inability to deliver it as fuel to organs and tissues. This, the researchers say, is the essence of diabetes.

Working with mice whose pancreatic cells were missing the EPAC2 signaling molecule, the researchers found that lean, healthy mice regulated their blood sugar levels even in the absence of EPAC2. Short-term surges in food consumption did not affect the mice's ability to regulate their blood sugar, but when the mice were put on a high-fat diet for a month, they developed a condition similar to human diabetes. At the same time, a group of overfed, pudgy mice with intact EPAC2 managed to control blood sugar levels without a problem. In other words, EPAC2 remained dormant and played no role in insulin production under normal conditions, but emerged as a critical factor when the fat mice needed more insulin to control their surging blood sugar levels. This finding led the scientists to believe EPAC2 is an important fail-safe mechanism unlocked only during abnormal conditions.

"It is as if during these extreme conditions, the body calls upon EPAC2 as backup to help it balance insulin supply and demand," Hussain says.

The study further reveals that EPAC2 is critical because it acts as a link in a signaling cascade that culminates in the release of insulin by pancreatic cells. Comparing E
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Contact: Ekaterina Pesheva
peshev1@jhmi.edu
410-502-9433
Johns Hopkins Medicine
Source:Eurekalert

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