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Uncoupling modifier genes from uncoupling protein 2 in pancreatic beta-cells.

Intracellular levels of oxygen and glucose are higher in pancreatic insulin-secreting β-cells than any other mammalian cell. Indeed, among endocrine secretory cells, the pancreatic β-cell is unique in using glucose catabolism to meet its energy needs while relying on glucose metabolism to generate appropriate signals to maintain insulin secretion and glucose homeostasis. The unabated and successful execution of these two independent functions over the lifetime of the β-cell, requires fine coordination between several families of intracellular proteins. In addition to glucose, the β-cell also responds to other nutrients (fatty acids and amino acids), hormones, and nerve signals. Given this barrage of stimuli, it is logical to imagine that the β-cell would be armed with appropriate defense mechanisms to prevent excess stress that could lead to eventual cell dysfunction and/or death. On the contrary, the β-cell is particularly weak against the toxicity of free radicals including reactive oxygen species (ROS) and reactive nitrogen species (1,2) and, being a secretory cell, is also susceptible to endoplasmic reticulum (ER) stress (3,4). Thus, understanding the mechanisms and pathways that mediate the effects of oxidative or ER stress (3) is important to understand β-cell biology and to plan therapeutic approaches to prevent β-cell dysfunction and death.