Response to Comment on: Allister et al. UCP2 Regulates the Glucagon Response to Fasting and Starvation. Diabetes 2013;62:1623–1633

  1. Michael B. Wheeler
  1. Department of Physiology, University of Toronto, Toronto, Ontario, Canada
  1. Corresponding author: Michael B. Wheeler, michael.wheeler{at}utoronto.ca.

We thank Dr. Gylfe (1) for his interest in our work showing a role for uncoupling protein 2 (UCP2) in regulating α-cell glucagon secretion and suggesting that this is an interesting and potentially important finding. We agree that the role and mechanism of glucose sensing in α-cells is still highly controversial and that two opposing models are promoted in the literature. Our data suggests that the presence of UCP2 in α-cells may play a role in glucose sensing because the absence of UCP2 impaired the release of glucagon, and this was accompanied by reduced mitochondrial membrane potential hyperpolarization, increased reactive oxygen species production, more depolarized plasma membrane potential, and lower intracellular calcium …

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