Cannabinoids Induce Pancreatic β-Cell Death by Directly Inhibiting Insulin Receptor Activation

Wook Kim, Qizong Lao, Yu-Kyong Shin, Olga D. Carlson, Eun Kyung Lee, Myriam Gorospe, Rohit N. Kulkarni, Josephine M. Egan*

*To whom correspondence should be addressed. E-mail: eganj{at}grc.nia.nih.gov

This PDF file includes:

• Fig. S1. CB1 receptor abundance in pancreatic β-cell lines.
• Fig. S2. Effects of ACEA depend on the CB1 receptor.
• Fig. S3. Effects of WIN55,212-2 on human hepatocarcinoma HepG2 cells and primary human hepatocytes.
• Fig. S4. Effects of Gα_i3 on insulin receptor signaling.
• Fig. S5. Improved β-cell mass due to enhanced β-cell survival in STZ-treated CB1R^–/– mice.
• Fig. S6. Enhanced insulin signaling in β cells of STZ-treated CB1R^–/– mice.
• Fig. S7. Increased phosphorylation of p27 at Ser¹⁰ and Thr¹⁵⁷ in islets of STZ-treated mice by CB1 receptor blockade.
• Fig. S8. Increased abundance of PDX-1, GLUT2, and glucokinase in β cells of STZ-treated CB1R^–/– mice.
• Table S1. Details of the antibodies used for immunoblotting, immunoprecipitation, and immunofluorescence studies.
  

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© 2012 American Association for the Advancement of Science