Figure 4: β-cell-specific deletion of p53 partially reverses glucose intolerance and defective GSIS in β-MDM2KO mice. | Nature Communications

Figure 4: β-cell-specific deletion of p53 partially reverses glucose intolerance and defective GSIS in β-MDM2KO mice.

From: The MDM2–p53–pyruvate carboxylase signalling axis couples mitochondrial metabolism to glucose-stimulated insulin secretion in pancreatic β-cells

Figure 4

Eighteen-week-old male β-MDM2KO mice (KO), β-MDM2–p53 DKO mice and its WT littermates were used. (a) Isolated islets were subjected to immunoblotting using an anti-MDM2, -p53 or -β-actin antibody. Representative immunoblot images from three independent experiments are shown. (b) GTT. (c) Serum insulin levels during the GTT in b. (d) ITT. (e) Static GSIS in the isolated islets as in Fig. 1g. Note that insulin content in the islets was similar among the three groups. (f) Glucose (20 mM)-stimulated intracellular ATP production in the isolated islets. The values are expressed as fold change over basal level (2.8 mM glucose). *P<0.05 (KO versus WT, n=5), #P<0.05 (KO versus DKO, n=5) (Student’s t-test). All data are represented as the mean±s.e.m.

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