Fig. 4

PRKD2 deficiency enhanced Insulin secretion and lead to IR in mice. a, b Insulin excursion during IPGTTs (a) and area under the curve of insulin (b) in mice with the indicated genotypes at 14 weeks of age. *p < 0.05, **p < 0.01, WT vs PRKD2^−/− (WT, n = 24; PRKD2^−/−, n = 27). c, d Glucose excursion during IPGTTs (c) and area under the curve of glucose (d) in mice with the indicated genotypes at 14 weeks of age. **p < 0.01, WT vs PRKD2^−/− (WT, n = 22; PRKD2^−/−, n = 28). e, f Western blots of total Akt and Akt phosphorylation at ser473 in liver from WT and PRKD2^−/− mice at age of 14 weeks old. *p < 0.05, WT vs PRKD2^−/−; ^###p < 0.001, basal vs insulin-treatment (n = 8/group). g, h Western blots of total Akt and Akt phosphorylation at ser473 in skeletal muscle from WT and PRKD2^−/− mice at the age of 14 weeks old. *p < 0.05, WT vs PRKD2^−/−; ^##p < 0.01,   basal vs insulin-treatment (n = 8/group). i, j Glucose excursion during ITTs (i) and area under the curve of glucose (j) in mice with the indicated genotypes at 14 weeks of age (WT, n = 16; PRKD2^−/−, n = 17). *p < 0.05, **p < 0.01, WT vs PRKD2^−/−. All data are represented as mean ± SEM, the significant difference between groups was assessed by the Student’s t-test