Johns Hopkins Scientists Find ‘Second Fiddle’ Protein Has Leading Role In Type 2

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Johns Hopkins Scientists Find ‘Second Fiddle’ Protein Has Leading Role In Type 2


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Old 04-14-2013, 11:52   #1
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Default Johns Hopkins Scientists Find ‘Second Fiddle’ Protein Has Leading Role In Type 2

Unusual Suspect: Johns Hopkins Scientists Find

A team of researchers at the Johns Hopkins Children’s Center has found that a protein long believed to have a minor role in type 2 diabetes is, in fact, a central player in the development of the condition that affects nearly 26 million people in the United States alone and counts as one of the leading causes of heart disease, stroke and kidney, eye and nerve damage.

Working with mice, the scientists discovered that a protein called EPAC2 — deemed a second-fiddle player up until now — is actually an important regulator of insulin that appears to work by nudging insulin-secreting cells of the pancreas to ramp up production of the sugar-regulating hormone when the body needs it most. Until now, EPAC2 was suspected of playing a merely supporting role as a signaling molecule, but scientists remained uncertain why and how that mattered, if at all.

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“Drugs that precision-target failing pancreatic cells and restore or boost their function have become the holy grail of diabetes research. We believe that our finding establishes a pathway to do just that,” says lead investigator Mehboob Hussain, M.D., a pediatric endocrinologist at the Johns Hopkins Children’s Center and a metabolism expert at the newly formed Johns Hopkins Diabetes Institute.

(snip)

“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 EPAC2-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.

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