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Protein palmitoylation helps to model the evolution of some forms of type 2 diabetes   

On February 7, Guifang Dong, PhD; Sangeeta Adak, PhD; Qiang Zhang, PhD; Chu Feng, MS; Li Yin, MD; Sarah Speck; Shuntaro Morikawa; Rie Asada, PhD; Fumihiko Urano, MD, PhD; Maria Remedi, PhD; Xiaochao Wei, PhD; Clay Semenkovich, MD; and collaborators had their work published in “Cell Metabolism.” 

“Hyperinsulinemia often precedes type 2 diabetes,” and palmitoylation, implicated in exocytosis, is reversed by a major depalmitoylation enzyme called acyl-protein thioesterase 1 (APT1). 

By using palmitoylation proteomics in mouse models, the authors findings suggested that APT1 is regulated in human islets and that the deficiency of APT1 causes β cell failure, due to insulin hypersecretion. Further stating, that their findings “model the evolution of some forms of human type 2 diabetes.” 

Guifang Dong, Sangeeta Adak, George Spyropoulos, Qiang Zhang, Chu Feng, Li Yin, Sarah L. Speck, Zeenat Shyr, Shuntaro Morikawa, Rie Asada Kitamura, Rahul S. Kathayat, Bryan C. Dickinson, Xue Wen Ng, David W. Piston, Fumihiko Urano, Maria S. Remedi, Xiaochao Wei, Clay F. Semenkovich. Palmitoylation couples insulin hypersecretion with β cell failure in diabetes. Cell Metabolism. Volume 35, Issue 2. 2023. Pages 332-344.e7. SSN 1550-4131. https://doi.org/10.1016/j.cmet.2022.12.012