Fig. 1: T1DM mice presented increased β-OHB levels and CaMKII-α kbhb in the hippocampus. | Communications Biology

Fig. 1: T1DM mice presented increased β-OHB levels and CaMKII-α kbhb in the hippocampus.

From: Hippocampal CaMKII-α β-hydroxybutyrylation induces memory deficits in mice with type 1 diabetes mellitus

Fig. 1

A–D Levels of blood glucose, liver β-OHB, blood β-OHB, and hippocampal β-OHB in mice treated with STZ or vehicle 4 days after injection (blood glucose: n = 7 per group; liver β-OHB: n = 6 per group; blood β-OHB: n = 6 per group; and hippocampal β-OHB: n = 6 per group). E Increase in the hippocampal β-OHB concentration in mice 4 to 28 days after injection of STZ (n = 6 per group). F Degree of exogenous CaMKII-α kbhb at the K42 and K267 sites in HT22 cells treated with LV expressing CaMKII-α or mutant CaMKII-α in the presence of β-OHB (CaMKII-α kbhb at the K42 and K267 sites: n = 3 per group). G Degree of kbhb at the K42 and K267 sites in the recombinant CaMKII-α protein after β-OHB-CoA treatment. H Degree of hippocampal CaMKII-α kbhb at the K42 and K267 sites in mice 4 to 28 days after injection of STZ (n = 6 per group). The data are presented as the means ± SEMs; unpaired t test or one-way ANOVA; **p < 0.01 and ****p < 0.0001. Veh: vehicle; STZ: streptozotocin; bhb: β-hydroxybutyrylation.

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