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

PAC2-deficient and normal pancreatic cells under a microscope, the investigators found that the EPAC2-deficient cells were unable to regulate calcium, a well-known catalyst that triggers the release of insulin into the blood. EPAC2 functioned as calcium's gatekeeper, the researchers say. In its absence, calcium did not reach the critical mass needed to initiate the release of insulin.

The researchers say it remains unclear whether type 2 diabetes damages EPAC2 directly or whether EPAC2 can coax the cells to crank out extra insulin only for so long and eventually gives up. Either way, Hussain says, targeting EPAC2 with drugs could ratchet up the beta cells' dwindling insulin production and nip, or even reverse, diabetes at its root.

Type 2 diabetes is the predominant form of the disease, accounting for more than 90 percent of all diabetes diagnoses. It is commonly associated with diet and lifestyle. Previously seen mostly in middle-aged and older adults, type 2 diabetes is now increasingly diagnosed in younger people and children, a phenomenon fueled by growing obesity rates, experts say.


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Contact: Ekaterina Pesheva
peshev1@jhmi.edu
410-502-9433
Johns Hopkins Medicine
Source:Eurekalert

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