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Fig. 6 | Cardiovascular Diabetology

Fig. 6

From: β Cell-specific deletion of guanylyl cyclase A, the receptor for atrial natriuretic peptide, accelerates obesity-induced glucose intolerance in mice

Fig. 6

The NP/GC-A system contributes to β-cell proliferation and cyclin-D2 expression in diet-induced insulin obesity. a, b Effects of ANP on cyclin-D2 mRNA expression in vitro. a Concentration–response curve. Pancreatic islets from control mice were cultured in the absence (saline, as vehicle) or presence of different ANP concentrations (0.1–100 nM) for 24 h. b Comparison of genotypes. Pancreatic islets from control and β GC-A KO mice were cultured in the absence (saline, as vehicle) or presence of 1 nM ANP for 24 h. Values are the ratio of cyclin-D2 mRNA level relative to β2 microglobulin, determined by quantitative RT-PCR and expressed as x-fold vs vehicle-treated control islets (6–8 samples per condition). c Morphometrical analyses of mean islet areas, the area of β-cells per islet and the number of β-cells per islet in pancreatic sections obtained from β GC-A KO and control littermates after 8 weeks of ND or HFD. Top, representative sections stained for insulin, glucagon and cell nuclei (with DAPI) (5 mice per genotype and condition, 3 sections per mouse). d Cyclin-D2 mRNA levels relative to β2 microglobulin in islets freshly isolated from β GC-A KO and control littermates after 8 weeks of ND or HFD. Expression levels were determined by quantitative RT-PCR and expressed as x-fold vs control mice receiving an ND (5 mice per genotype and condition, 2 islet sample preparations/mouse). *P < 0.05 vs ND; #P < 0.05 vs control mice

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