A Neutral Look At AZD9291

Cd was found to alter insulin release from ��-pancreatic cells. In vitro studies on mouse renal cortical cells showed that Cd decreased both glucose uptake and expression of SGLT1, an Na+-dependent glucose symporter (Blumenthal et al., 1998). These results corroborated the studies on Cd-treated rats showing that Cd elevated activities of enzymes PR-171 in vivo responsible for gluconeogenesis in kidney tissue (Chapatwala, et al., 1982). Treatment of the Cd-intoxicated mice with monensin in the present study attenuated the Cd-induced increase of glucose concentration in serum. Figure 4 Glucose concentration in serum of the experimental animals. Each column represents mean��SD, n=6; Asterisk (*) represents significant differences between the Cd-treated group and normal controls, p always correlate with alteration of the lipid profile. The authors concluded that Cd exerted its atherogenic activity by causing endothelial damage (Messner et al., 2009). Figure 5 Lipid profile in serum of the experimental animals. Each column represents mean��SD, n=6; Asterisk (*) represents AZD9291 manufacturer significant differences between the Cd-treated group and normal controls, pYES1 and renal tissues revealed that treatment of Cd-intoxicated mice with monensin significantly improved the morphology of both organs studied (data not shown). The data from the atomic absorption analysis showed that the highest Cd concentrations were measured in the kidneys and hearts of the Cd-treated animals (second group) (Figures 6 and ?and7).7). The values for the concentration of Cd in both organs are higher than those reported in our previous study where the animals were subjected to 10 mg/kg Cd(II) acetate daily treatment for 2 weeks (Ivanova et al., 2012). The data presented in this study confirmed that accumulation of Cd in the organs was dose dependent. Monensin decreased the Cd concentration in the kidneys and heart of Cd-intoxicated animals by 57 and 64%, respectively (p