title: Data of intracellular insulin protein reduced by autophagy in INS-1E cells.
abstract: Autophagy appears to be involved in maintaining normal intracellular insulin content by accelerating the insulin degradation rate in β-cells (Marsh et al., 2007) [1]. 2-deoxy-d-glucose (2-DG) is metabolized by hexokinase, and acts as an inhibitor of glycolysis. 2-DG triggers glucose deprivation without altering other nutrients or metabolic pathways (Aghaee et al., 2012) [2], and appears to be an ideal tool for studying autophagy. Rapamycin induced upregulation of autophagy in both cultured isolated islets and pancreatic β-cells (Tanemura et al., 2012) [3]. Here, we examined that 2-DG or rapamycin-induced autophagy may decrease the production of intracellular insulin in INS-1E insulinoma cells. Data showed that autophagy was increased by 2-DG or rapamycin by Western blotting and Immunofluorescence staining analyses. Also, intracellular insulin decreased by 2-DG or rapamycin. Furthermore, the autophagy inhibitors, bafilomycin A1 and/or 3-methyladenine, in the presence or absence of 2-DG or rapamycin increased intracellular insulin in INS-1E insulinoma cells.
authors.affiliation: Department of Biomedical Engineering, Yonsei-Fraunhofer Medical Device Laboratory, Yonsei University, Wonju, Gangwon-do 26493, Republic of Korea.
authors.forename: Han Sung
authors.initials: HS
authors.lastname: Kim
authors.affiliation: Department of Biomedical Engineering, Yonsei-Fraunhofer Medical Device Laboratory, Yonsei University, Wonju, Gangwon-do 26493, Republic of Korea.
authors.forename: Yeong-Min
authors.initials: YM
authors.lastname: Yoo
keywords: 2-Deoxy-D-glucose; Autophagy; INS-1E Insulinoma cells; Insulin; Rapamycin