Seed germination and subsequent seedling development are critical phases in plants. These processes are regulated by a complex molecular network in which sugar has been reported to play an essential role. However, factors affecting sugar responses remain to be fully elucidated. In this study, we demonstrate that AtIPK2β, known to participate in the synthesis of myo-inositol 1,2,3,4,5,6-hexakisphosphate (IP6, phytate), affects Arabidopsis responses to glucose during seed germination. The loss-of-function mutant atipk2β showed increased sensitivity to 6% glucose and paclobutrazol (PAC). Yeast two-hybrid assay showed that AtIPK2β interacts with sucrose non-fermenting-1-related protein kinase (SnRK1.1), and bimolecular fluorescence complementation (BiFC) and pull-down assay further confirmed this interaction. Moreover, AtIPK2β was phosphorylated by SnRK1.1 in vitro, and the effect of restoring AtIPK2β to yeast cells lacking IPK2 (Δipk2) was abolished by catalytically active SnRK1.1. Further analysis indicated that IP6 reduces the suppression of seed germination caused by glucose, accompanied by altered expression levels of glucose-/hormone-responsive genes. Collectively, these findings indicate that AtIPK2β and IP6 are involved in glucose suppression of seed germination and that AtIPK2β enzyme activity is likely to be regulated by SnRK1.1.