HNF4A intestinal epithelial conditional loss incidence on jejunum expression from mice fed a HFD.
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ABSTRACT:
PROVIDER: PRJNA613038 | ENA |
REPOSITORIES: ENA
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Project description:HNF4A encodes a nuclear receptor required for the development of the intestine and involved in the homeostasis maintenance of intestinal epithelial cells during the adulthood. Also strongly related to the hepatic lipid metabolism, little was known about its metabolic relevance from the intestine when challenged by a high fat diet. We used microarrays to detail the global programme of jejunal gene expression depending on HNF4α and influenced by HFD.
2020-03-18 | GSE147105 | GEO
Project description:Purpose: To investiagte why maternal obesity induces the susceptibility of offspring to diethylnitrosamine (DEN)-induced hepatocellular carcinoma (HCC) over generations upon over nutrition.The goals of this study are to find over-generationally altered genes and miRNAs which may contribute the accumulative progeny susceptibility to HCC under over nutrition. Methods: C57BL/6 female mice (F0 generation) were fed with either normal chow (NC) or HFD (60% kcal fat) from 1-month to 3-month old, and mated with NC-fed male mice to produce F1 generation. The F2 generation was similarly created. Male offspring of the F0, F1 and F2 generations were intraperitoneally injected with DEN at 2-weeks-old, and kept inmaintained on HFD and named as H1D, H2D and H3D groups, respectively. Male offspring of the F0 generation injected with PBS (Nor group) or DEN (NCD group) at the same age and kept inmaintained on NC. All groups were sacrificed at 40-weeks-old. Liver mRNA profiles and miRNA profiles from the different offspring groups were generated by LncRNA sequencing and small RNA sequencing. Results: We identified many over-generationally changed genes and miRNAs in the offspring by RNA-sequencing. Conclusions: The study revealed an important role of miRNA and targeting genes in regulating the incidence of HCC in the offspring of maternal-lineage under multi-generational HFD exposure, which has a profound effect on exploring the link between maternal obesity and the development of diseases in offspring.
2021-07-01 | GSE117539 | GEO
Project description:Maternal multi-generational high fat diet (HFD) exposure increases the offspring HCC incidence
| PRJNA482414 | ENA
Project description:RNAseq of osteocyte and osteoblasts enriched bone fraction from the tibiae of 6 week-old male mice with a conditional deletion of Hnf4a in osteoblasts and and WT littermates.
2023-06-07 | GSE190313 | GEO
Project description:To understand how HNF4A loss affects gene expression in mouse liver. We used control and HNF4A KO mouse livers for RNA sequencing. In addition, we also examined the effect of HNF4A gain in mouse fibroblast cells by ectropically expressing HNF4A in NIH3T3 cell to identify genes that are regulated by HNF4A.
2024-01-15 | GSE210842 | GEO
Project description:Obesity is an established risk factor for cancer in many tissues such as the gastrointestinal tract. In the mammalian intestine, a pro-obesity high fat diet (HFD) promotes tumorigenesis in part by enhancing intestinal stem cell (ISC) numbers, proliferation and function. Although Ppar (Peroxisome proliferator-activated receptor) nuclear receptor activity has been proposed to mediate some of these effects in HFD ISCs, the exact role that different Ppar family members play in this process is unclear. Here, we find that in loss-of-function in vivo models, both Ppar family members alpha and delta contribute to the HFD response in ISCs. Mechanistically, both PPARs do so by robustly inducing a downstream fatty acid oxidation (FAO) metabolic program. Notably, pharmacologic and genetic disruption of CPT1a (the rate limiting enzyme of FAO) blunts the HFD phenotype in ISCs. Furthermore, just as HFD ISCs depend on CPT1a-mediated FAO, inhibition of CPT1a dampens the pro-tumorigenic consequences of a HFD on early tumor incidence and progression in the intestine. These findings demonstrate that inhibition of a HFD activated FAO program creates a therapeutic opportunity to counter the effects of a HFD on ISCs and intestinal tumorigenesis.
2021-06-01 | GSE151045 | GEO
Project description:Obesity is an established risk factor for cancer in many tissues such as the gastrointestinal tract. In the mammalian intestine, a pro-obesity high fat diet (HFD) promotes tumorigenesis in part by enhancing intestinal stem cell (ISC) numbers, proliferation and function. Although Ppar (Peroxisome proliferator-activated receptor) nuclear receptor activity has been proposed to mediate some of these effects in HFD ISCs, the exact role that different Ppar family members play in this process is unclear. Here, we find that in loss-of-function in vivo models, both Ppar family members alpha and delta contribute to the HFD response in ISCs. Mechanistically, both PPARs do so by robustly inducing a downstream fatty acid oxidation (FAO) metabolic program. Notably, pharmacologic and genetic disruption of CPT1a (the rate limiting enzyme of FAO) blunts the HFD phenotype in ISCs. Furthermore, just as HFD ISCs depend on CPT1a-mediated FAO, inhibition of CPT1a dampens the pro-tumorigenic consequences of a HFD on early tumor incidence and progression in the intestine. These findings demonstrate that inhibition of a HFD activated FAO program creates a therapeutic opportunity to counter the effects of a HFD on ISCs and intestinal tumorigenesis.
2021-06-01 | GSE151046 | GEO
Project description:Tamoxifen-inducible conditional knockout (CKO) mice were generated to explore the function of Gcn1 in adult mice using the Cre/loxP system. To analyze the function of GCN1 in the intestinal epithelium, we compared the whole cell proteome of jejunum harvested from GCN1 CKO mice with that of wild-type mice.
2022-08-29 | PXD030519 | JPOST Repository