Session: SAT 389-413-Signaling and Transcriptional Control in Endocrine Systems
Poster Board SAT-412
Methods: Virgin Wistar rats were divided into two dietary groups of 5 rats each and fed ad libitum from 3 week preconception to 21 day postparturition. Rats in the first group were fed a control diet (0.90% Ca) and rats in the second group were fed a Ca-deficient diet (0.008% Ca). One female and 1 male offspring were selected from each of the 5 litters by random removal on day 21 and killed. Methylation of cytosine-guanine (CpG) dinucleotides in the phosphoenolpyruvate carboxykinase (Pck1), peroxisome proliferator-activated receptor a (Ppara), glucocorticoid receptor (Nr3c1), 11β-hydroxysteroid dehydrogenase-1 (Hsd11b1), and 11β-hydroxysteroid dehydrogenase-2 (Hsd11b2) promoters was measured in liver tissue using pyrosequencing. For each gene, quantitative real-time PCR was used to assess mRNA levels in liver tissue.
Results: There were no significant differences in birth weight or body weight between groups at day 21. No significant difference between the groups was observed in blood pressure, serum ionized Ca level. Serum corticosterone levels of male pups from the Ca-deficient dams were high as compared to their counterparts, while no significant difference was observed in female. Serum insulin levels of female pups from the Ca-deficient dams were lower than that from control dams. The methylation levels of all genes did not differ between groups, except for that of Hsd11b1, which was lower in the Ca-deficient group. Expression of Pck1 and Nr3c1 was lower in the Ca-deficient group than the control group.
Conclusions: A Ca-deficient diet for a dam during gestation and early nursing may alter glucocorticoid metabolism and lead to higher intracellular glucocorticoid concentration in hepatic cells of her offspring, and this abnormal glucocorticoid metabolism may induce the metabolic complications associated with Ca deficiency.
Nothing to Disclose: JT, AI, KK
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