Figure 1: Effects of β-cell-specific deletion of MDM2 on glucose homeostasis and insulin secretion in mice. | Nature Communications

Figure 1: Effects of β-cell-specific deletion of MDM2 on glucose homeostasis and insulin secretion in mice.

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

Figure 1

(a) Immunofluorescence staining of MDM2 (red) and VAMP2 (as a β-cell marker) (green) in pancreatic sections of 6-week-old male β-cell-specific MDM2 knockout (β-MDM2KO) mice and its WT littermates with original magnification at × 400. (b) Pancreatic islets and exocrine (Exo) cells isolated from the above mice were subjected to immunoblotting using an antibody against MDM2, p53, β-actin or VAMP2 as indicated. The right panel is the densitometric analysis for the relative abundance of MDM2 and p53 normalized with β-actin. (c–h) Twelve-week-old male β-MDM2KO mice, WT littermates and RIP-Cre controls were used (n=6). (c) GTT. (d) Serum insulin levels during the GTT in panel C. (e) ITT. (f) Serum insulin levels on L-arginine stimulation. (g) The isolated islets were stimulated with glucose (20 mM) or KCl (20 mM) for 30 min, followed by measurement of insulin concentration in the conditional medium (n=5). (h) Dynamic insulin secretion of the isolated islets in response to glucose stimulation (10 mM) using a perfusion system (n=4). Note that the islets were maintained in the conditional medium with 2.8 mM glucose as basal levels and the insulin content of the isolated islets was comparable between the three genotypes. All experiments were repeated at least four times and representative images are shown. *P<0.05 (KO versus WT), #P<0.05 (KO versus Cre control) (Student’s t-test). Scale bar, 50 μm. All data are represented as the mean±s.e.m.

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