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Maternal multi-generational high fat diet (HFD) exposure increases the offspring HCC incidence

ABSTRACT: Maternal multi-generational high fat diet (HFD) exposure increases the offspring HCC incidence

PROVIDER: PRJNA482414 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7554860_1.fastq.gz	Fastqsanger.gz
	SRR7554860_2.fastq.gz	Fastqsanger.gz
	SRR7554870.fastq.gz	Fastqsanger.gz
	SRR7554861_1.fastq.gz	Fastqsanger.gz
	SRR7554861_2.fastq.gz	Fastqsanger.gz

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Maternal multi-generational high fat diet (HFD) exposure increases the offspring HCC incidence

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

Single cell RNA-seq mapping of chronological obesity-HCC progression in C57BL/6 mice fed a CD-HFD

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2024-02-17 | GSE232182 | GEO

HNF4A intestinal epithelial conditional loss incidence on jejunum expression from mice fed a HFD.

Project description:HNF4A intestinal epithelial conditional loss incidence on jejunum expression from mice fed a HFD.

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Multigenerational paternal high-fat diet gradually exacerbates environmental stress-induced testicular dysregulated expression of mRNAs in offspring

Project description:To investigate the mechanism by which paternal exposure to high-fat diet (HFD) exacerbates environmental stress-impaired testicular germ cell development in offspring, testicular RNA sequencing was performed in H+Cd (the offspring were treated with Cd after paternal exposure to one-generational HFD) and H+H+Cd (the offspring were treated with Cd after paternal exposure to bi-generational HFD) groups. Compared with HFD1D group and HFD2D group, 229 mRNAs were upregulated and 268 mRNAs were downregulated, screened for a 1.2-fold change and adjusted with P < 0.05. GO analysis revealed that downregulated mRNAs were related to multiple biological processes, including the "retinol metabolic process," the "reproductive process," and the "spermatogenesis".

2023-12-22 | GSE241413 | GEO

Single cell RNA-seq of single cell suspension from the HCC region of mice fed CD-HFD for 15 mice and treated with FABP5 inhibitor or control

Project description:We perform scRNA-seq in the livers of C57BL/6 mice fed a CD-HFD for 15 months. Starting from the 13M, mice were treated with FABP5 inhibitor to ameliorate HCC.

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HNF4A intestinal epithelial conditional loss incidence on jejunum expression from mice fed a HFD.

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.

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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.

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HFD activated FAO mediates intestinal stemness and tumorgenicity II

2021-06-01 | GSE151046 | GEO

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Project description:Obesity is a global health concern affecting over 650 million adults with a major contributor being an increased consumption of a high-fat diet. Maternal obesity often results in an increased risk of offspring developing obesity. In this study, we examined the effect of diet on visceral adipose in a pre-clinical model of generational diet-induced obesity that included maternal cohorts of C57BL/6 mice fed either a control diet (10% fat) or a high-fat diet (45% fat) and the resulting female offspring fed either diet. Using bottom-up proteomics on omental adipose tissue, differential protein expression was determined with the greatest difference resulting from the generational obese cohort. Differentially expressed proteins were involved in pathways related to cancer, inflammatory disease and immune response. Taken together, the results of this study provide molecular-level insight that will enable the development of more targeted, modifiable interventions that could be implemented pre-, during and post-pregnancy.

2024-10-17 | PXD042092 | Pride

Investigation of mechanism using highly intrahepatic metastatic cell lines of HCC

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