Fig. 1: DNAJA2 deficiency disrupts the homoestasis of glucose metabolism in mice. | Nature Communications

Fig. 1: DNAJA2 deficiency disrupts the homoestasis of glucose metabolism in mice.

From: Heat shock protein DNAJA2 controls insulin signaling and glucose homeostasis by preventing spontaneous insulin receptor endocytosis

Fig. 1

A Morphologies of wild-type (WT), DNAJA2 heterozygous (DJ2+/−) and knockout (DJ2−/−) littermates at birth (P0). Arrows indicate milk spots. B Representative images of H&E staining and periodic acid-Schiff (PAS) staining of livers from WT and DJ2−/− newborns. Scale bar, 100 μm. n = 2 experimental repeats. C Liver glycogen levels in WT (n = 5) and DJ2−/− (n = 4) newborns. D Liver glycogen levels in 2-month-old WT (n = 10) and liver-specific DNAJA2 knockout (CKO) mice (n = 13). E Fed blood glucose levels of WT (n = 43) and CKO mice (n = 36) at 2-month-old. F Serum insulin levels in WT and CKO mice at 2-month-old (n = 20). Glucose tolerance (G) and insulin tolerance (H) tests in 2-month-old WT (n = 25, 18) and CKO mice (n = 22, 14). I Glycogen synthase activity of WT and CKO livers treated with insulin (1 U/kg body weight) for 10 min (n = 3). Data are shown as means ± SEM. P values were determined by two-tailed unpaired t test with Welch’s correction. *p < 0.05; **p < 0.01; ***p < 0.001, ****p < 0.0001. Source data are provided as a Source Data file.

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