Figure 6.

Inhibition of insulin secretion by IGF-1 is accompanied by a decrease in cAMP. HIT-T15 cells were preincubated with Krebs–Ringer buffer containing no glucose for 1 hr before treatment with GLP-1 and/or IGF-1 in the presence of glucose at a high concentration. Different conditions are represented by different stippling patterns. GLP-1, as expected, increased cAMP and potentiated insulin secretion from the HIT-T15. IGF-1 counteracted the GLP-1 effect on insulin secretion and caused a drop in cAMP.