Skip to main content

Advertisement

Fig. 1 | Cardiovascular Diabetology

Fig. 1

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

Fig. 1

Deletion of GC-A in β-cells from GC-Afl/fl; RipCretg (β GC-A KO) mice. a PCR analysis. Genomic DNA from different tissues was assayed for the appearance of the ~ 700-bp amplicon which results from complete recombination of the floxed GC-A gene segment. Genomic DNA was from white adipose tissue (WAT), skeletal muscle (Sk M), isolated pancreatic islets and hearts. b Quantitative RT-PCR analysis. GC-A mRNA expression levels in pancreatic islets from control and β GC-A KO mice. Values are the ratio of GC-A mRNA level relative to β2 microglobulin, expressed as x-fold vs control islets (20 samples per genotype). c Cyclic GMP determinations. Concentration-dependent effects of ANP on intracellular cGMP contents of pancreatic islets prepared and cultured from control mice (15 min incubation in the presence of the phosphodiesterase inhibitor IBMX; n = 4 per condition). d Comparison of the cGMP responses of β GC-A KO and control islets to 100 nM ANP (15 min incubation in the presence of IBMX; n = 4 per genotype and condition). e Insulin release. Effects of ANP on glucose-dependent insulin secretion by pancreatic islets prepared from β GC-A KO and control littermates (1 h incubation; n = 4). f Systolic, mean and diastolic arterial blood pressure levels of β GC-A KO and control littermates (n = 16 per genotype). *P < 0.05 vs vehicle; #P < 0.05 vs controls

Back to article page