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Translatomics probes into the role of lycopene on improving hepatic steatosis induced by high-fat diet

ABSTRACT: Translatomics probes into the role of lycopene on improving hepatic steatosis induced by high-fat diet

PROVIDER: PRJNA738497 | ENA |

REPOSITORIES: ENA

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Translatomics probes into the role of lycopene on improving hepatic steatosis induced by high-fat diet

Project description:Liver is an important organ for fat metabolism. Excessive intake of a high-fat/energy diet is a major cause of hepatic steatosis and its complications such as nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Supplementation with lycopene, a natural compound, is effective in lowering triglyceride levels in the liver, although the underlying mechanism at the translational level is unclear. In this study, mice were fed a high-fat diet (HFD) to induce hepatic steatosis and treated with or without lycopene. Translation omics and transcriptome sequencing were performed on the liver to explore the regulatory mechanism of lycopene in liver steatosis induced by HFD, and identify differentially expressed genes (DEGs).

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Project description:We performed translatome and transcriptome sequencing (RNC-seq and RNA-seq) on the livers of normal chow diet-, high-fat diet- and High-fat diet plus lycopene-fed mice.

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oyster mushroom against hepatic steatosis in obese Zucker rats

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Microarray examination of liver tissue from mice fed 58% saturated high fat diet to induce hepatic steatosis.

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Project description:Pyrimidine catabolism is implicated in hepatic steatosis. Dihydropyrimidine Dehydrogenase (DPYD) is an enzyme responsible for uracil and thymine catabolism, and DPYD human genetic variability affects clinically observed toxicity following 5-Fluorouracil (5-FU) administration. In an in vitro model of diet-inducedfatty acid-induced steatosis, the pharmacologic inhibition of DPYD resulted in protection from lipid accumulation. Additionally, a gain-of-function mutation of DPYD, created through clustered regularly interspaced short palindromic repeats associated protein 9 (CRISPR-Cas9) engineering, led to an increased lipid burden, which was associated with altered mitochondrial functionality in a hepatocarcionma cell line. The studies presented herein describe a novel role for DPYD in hepatocyte metabolic regulation as a modulator of hepatic steatosis.

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Intestinal NSD2 aggravates hepatic steatosis during obesity through histone modifications [CUT&Tag]

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