Abstract
A growing body of evidence suggests that the insulin-producing beta cells in the pancreas are susceptible to saturated fatty acid-induced endoplasmic reticulum (ER) stress and apoptosis, and that this may contribute to the development of diabetes. In this issue of the European Journal of Lipid Science and Technology, Guo et al. [p. 233–234] report on accelerated beta cell dysfunction and death induced by high fat feeding of the Ncb5or knockout mouse, which lacks the ER-associated NADH-cytochrome b5 oxidoreductase and has impaired fatty acid desaturation.
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