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Microarray analysis of developmentally programmed hepatic steatosis in Undernourishment in utero mouse model

ABSTRACT: Microarray analysis of developmentally programmed hepatic steatosis in Undernourishment in utero mouse model

PROVIDER: PRJNA509660 | ENA |

REPOSITORIES: ENA

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Microarray analysis of developmentally programmed hepatic steatosis in Undernourishment in utero mouse model

Project description:Nutritional imbalances in the early developmental period have an impact on the long-term risk of developing non-alcoholic fatty liver disease (NAFLD). In the present study, we demonstrated that tauroursodeoxycholic acid (TUDCA), a secondary bile acid, and markedly ameliorated hepatic steatosis in a mouse model of undernourishment in utero. Herein, we studied the effect of maternal caloric restriction on genetic expression by microarray analysis among 3 different time points of independent cohorts. Cohort 1 (at 9 weeks; without HFD), cohort 2 (at 17 weeks; with HFD), and cohort 3 (at 22 weeks; HFD with or without the TUDCA treatment) (Muramatsu-Kato et al., 2015). We compared the alteration in gene expression between NN pups and UN pups before and after postnatal high-fat diet (HFD) at 9 weeks and 17 weeks. Later we studied the TUDCA treatment responce on NN pups and UN pups.

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Plasticity of histone modifications around Cidea and Cidec genes with secondary bile in the amelioration of developmentally-programmed hepatic steatosis.

Project description:We recently reported that a treatment with tauroursodeoxycholic acid (TUDCA), a secondary bile acid, improved developmentally-deteriorated hepatic steatosis in an undernourishment (UN, 40% caloric restriction) in utero mouse model after a postnatal high-fat diet (HFD). We performed a microarray analysis and focused on two genes (Cidea and Cidec) because they are enhancers of lipid droplet (LD) sizes in hepatocytes and showed the greatest up-regulation in expression by UN that were completely recovered by TUDCA, concomitant with parallel changes in LD sizes. TUDCA remodeled developmentally-induced histone modifications (dimethylation of H3K4, H3K27, or H3K36), but not DNA methylation, around the Cidea and Cidec genes in UN pups only. Changes in these histone modifications may contribute to the markedly down-regulated expression of Cidea and Cidec genes in UN pups, which was observed in the alleviation of hepatic fat deposition, even under HFD. These results provide an insight into the future of precision medicine for developmentally-programmed hepatic steatosis by targeting histone modifications.

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