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. Author manuscript; available in PMC: 2019 Aug 1.
Published in final edited form as: J Nutr Biochem. 2018 May 12;58:59–70. doi: 10.1016/j.jnutbio.2018.04.018

Fig. 1.

Fig. 1

Genistein activated cAMP signaling via a Gαs-mediated mechanism in β-cells. (A) AC activity in INS1 cell plasma membranes preincubated with 100 μM GDPβS (A), Gαs antibody (Gαs, 1:200 (B), nonimmune IgG, or vehicle (V) for 30 min at 25°C, followed by stimulation with genistein (G, 2.5 μM), GLP-1 (GLP, 20 nM), forskolin (Fsk, 5μM) or vehicle for 10 min. Intracellular cAMP levels in INS1 cells (C) or human islets (D) pretreated with Gαs inhibitor mellittin (M, 5μM) for 30 min, followed by stimulation with genistein (G, 5μM) for 20 min. Islets were infected with lentiviral particles containing Gαs shRNA (Gαsh) or control shRNA (Csh) at MOI of 150. 48 h later, control and infected islets were either lysed for measuring Gαs and β-actin protein expression to determine the efficiency of knockdown (E), or incubated with genistein (G, 5μM) for 20 min to measure intracellular cAMP levels (F). Cyclic AMP levels were normalized to the protein contents, and expressed as percentage of the control value. Data are mean±SEM (n=4). *, p<0.05 vs. control.