Skip to main content
. 2009 Feb;150(2):580–591. doi: 10.1210/en.2008-0726

Fig. 5.

Fig. 5.

Effect of PI3 kinase-Akt and MEK-ERK1/2 inhibition on insulin-mediated GLP-1 secretion. GLUTag (A and C) and NCI-H716 (B and D) cells were pretreated with 50 μm LY294002 (A, n = 4–5/group; B, n = 6/group) or 50 μm PD98059 (C, n = 6–9/group; D, n = 5–6/group) for 15 min and subsequently treated with 10−8 or 10 −7 m insulin, respectively, for 2 h. GLP-1 secretion was determined by RIA, and all data were expressed as a percent of the untreated control. Insets, PI3 kinase inhibitory activity of the LY294002 was confirmed by immunoblot analysis of Akt phosphorylation in response to insulin in both cell models (n = 4/group). *, P < 0.05, ***, P < 0.001 when compared with untreated control; #, P < 0.05, ##, P < 0.01, ###, P < 0.001 as indicated.