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Scheuner et al. (2005) studied glucose homeostasis in mice with a ser51-to-ala substitution at the phosphorylation site Whiteville NC cash with bad credit of the translation initiation factor eIF2-alpha (see 603907 ) and observed that heterozygous mutant mice became obese and diabetic on a high-fat diet. Profound glucose intolerance resulted from reduced insulin secretion accompanied by abnormal distention of the ER lumen, defective trafficking of proinsulin, and a reduced number of insulin granules in beta cells. Scheuner et al. (2005) proposed that translational control couples insulin synthesis with folding capacity to maintain ER integrity and that this signal is essential to prevent diet-induced type II diabetes.