Experience

Marine Biological Laboratory

 

Supervisor: Dr. Peter J.S. Smith

 

Project: Electrical coordination between distinct sites in the pancreas coincides with pulsatile insulin secretion in mice.

 

Our previous studies have shown that uncoupling protein-2 (UCP2) can negatively regulate glucose-stimulated insulin secretion (GSIS) and likely does so by limiting the glucose-stimulated increase in ATP production in the pancreatic b-cell.  UCP2 catalyzes a proton leak across the mitochondrial inner membrane, thereby dissipating the proton-motive force and preventing ATP production.  Since UCP2 can uncouple oxidative phosphorylation, then it may also alter the requirement for oxygen in a glucose-dependent manner.  We now show that UCP2 knockout (-/-) mouse islets have lower basal and glucose-stimulated oxygen consumption.  UCP2 (-/-) islets also display faster oscillations in oxygen consumption than wild type islets and this occurs in a glucose-dependent fashion, suggesting that UCP2 may also be involved in regulating oscillations in insulin secretion.  This is not unexpected because the activity of UCP2 will determine the availability of protons to drive ATP production by ATP synthase.  Our current data suggest the possibility that UCP2 may modulate the oscillatory pattern of ATP production and thus oscillations in K_ATP channel activity, plasma membrane potential and insulin secretion.

 

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