Fig. 3.
Regulation of CAMP gene expression in vitro in differentiated 3T3-L1 adipocytes. CAMP mRNA was measured by quantitative real-time PCR. CAMP, Cathelicidin anti-microbial peptide; GAPDH, glyceraldehyde-3-phosphatedehydrogenase. Panel a : High concentrations of glucose and insulin synergistically suppress the gene expression of CAMP in adipocytes in vitro. Differentiated 3T3-L1 adipocytes were incubated under varying glucose and insulin concentrations. Cells were exposed to low/normal (low Glc/LGlc) glucose concentrations (5.6 mM) and to supraphysiologic (high Glc/HGlc) glucose concentrations (25 mM) alone or in combination with low (0.2 nM) and high (2.0 nM) insulin (Ins) concentrations for 18 h. n=10–12 wells were investigated per experimental setting. The combined exposure to high glucose and high insulin concentrations significantly reduced CAMP gene expression (p=0.004; Kruskal–Wallis test). Panel b : Effects of bile acids on CAMP expression in adipocytes in vitro. Differentiated 3T3-L1 adipocytes were exposed to a broad panel of bile acids. Tauromuricholic acid (TMCA; 1 and 10 μM), taurohyodeoxycholic acid (THDCA; 10 μM), cholic acid (CA; 10 and 100 μM), deoxycholic acid (DCA; 1 and 10 μM), and taurodeoxycholic acid (TDCA; 1 and 10 μM) were investigated. °p<0.05; * p<0.01 (Kruskal–Wallis test). n=6 wells were investigated per experimental setting. Panel c : Effect of GLP-1 on CAMP expression in adipocytes in vitro. GLP-1 significantly (p=0.007) inhibited CAMP gene expression (Kruskal–Wallis test). GLP-1: Glucagon-like peptide-1; Ctrl.: Control. n=8–12 wells were investigated per experimental setting. Panel d : Effects of testosterone and estradiol on CAMP expression in adipocytes in vitro. Neither testosterone nor estradiol significantly (Kruskal–Wallis test) influenced CAMP expression. Test.: Testosterone; Est.: Estradiol; n=6–12 wells were investigated per experimental setting.