No differences between the four fructose-fed groups were seen regarding

the VX-809 chemical structure initial body weight recorded prior to the intervention (p = 0.83, Table 2). Neither did the weight at the time of termination of the experiment (p = 0.84), nor the weight gain during the intervention (p = 0.68), differ between the four groups. No differences were found between the four groups regarding the weight of the fat pad (p = 0.32), and MRI showed no differences in total or visceral adipose tissue volumes between the four groups (see Table 2 for details). However, MRI revealed a greater fat infiltration in the liver of BPA-exposed rats than in the fructose-fed control rats. In the medium-dose and the high-dose group of BPA exposed rats the liver fat content was higher when compared with the fructose control group (p = 0.011, medium dose; p = 0.012, high dose). The lowest dose of BPA did not significantly influence liver fat content ( Fig. 3). Also the MRI liver R2* analysis showed an

effect on the liver by BPA, being significant in all three groups when compared one by one to the fructose control group (low-dose; p = 0.0008, middle-dose; p < 0.0001, high-dose; p = 0.0161, Table 2). A similar picture emerged, although not as pronounced as for the R2* signal, when the liver somatic index (LSI) was investigated. LSI was increased in the low-dose (p = 0.043, not significant following Bonferroni adjustment) and middle-dose group (p = 0.018, not significant following Bonferroni adjustment), but not significantly so buy Z-VAD-FMK in the high-dose group when compared with the fructose-fed control rats ( Table 2). Both the medium-dose and high-dose of BPA groups showed significantly higher levels of plasma apo A-I, when compared with the fructose control group (p < 0.0001, medium dose; p < 0.0001 high dose). The lowest dose of BPA did not cause any significant difference in apo A-I ( Fig. 4). Plasma cholesterol and plasma triglycerides were not significantly altered by the BPA exposure. Neither was blood

glucose at week 9, or ASAT and ALAT altered by BPA exposure. Of all variables studied (see Table 2), only plasma triglycerides and LSI were significantly increased by fructose feeding alone when compared to the water-fed control p = 0.0011 and p = 0.0031, respectively. The present study disclosed no evidence that BPA exposure in juvenile female fructose-fed F of 344 rats would increase fat mass, despite the use of both weights and MR imaging based detailed quantification of different adipose tissue compartments. However, the observed increase in liver fat infiltration, detected by MRI in parallel with increase in LSI, although in the latter case not significant following strict Bonferroni correction for multiple testing, even at dosages close to TDI, is a finding that warrants further investigations. Interestingly, an increase in liver fat infiltration appeared at the middle dose, but was not further increased at the highest BPA dose.