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Effect of sarsasapogenin (SAR) on non-alcoholic fatty liver disease in mice fed with methionine choline deficiency (MCD) diet

ABSTRACT: Effect of sarsasapogenin (SAR) on non-alcoholic fatty liver disease in mice fed with methionine choline deficiency (MCD) diet

PROVIDER: PRJNA924059 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23085826_1.fastq.gz	Fastqsanger.gz
	SRR23085826_2.fastq.gz	Fastqsanger.gz
	SRR23085827_1.fastq.gz	Fastqsanger.gz
	SRR23085827_2.fastq.gz	Fastqsanger.gz
	SRR23085828_1.fastq.gz	Fastqsanger.gz

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Effect of sarsasapogenin (SAR) on non-alcoholic fatty liver disease in mice fed with methionine choline deficiency (MCD) diet

Project description:This study aimed to investigate the effects and underlying mechanisms of sarsasapogenin (SAR) on dietary methionine choline deficiency induced non-alcoholic fatty liver disease in mice, The differentially expressed genes in liver tissue in “Normal VS model ”and “Model VS SAR” were identified by RNA-seq.

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Transcription profiling by array to identify the effects of n-3 polyunsaturated fatty acids on non-alcoholic steatohepatitis in mice

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Project description:Choline and methionine/choline deficient diets are widely used to generate severe rodent hepatic steatosis and steatohepatitis in an attempt to reflect stages of human non-alcoholic fatty liver disease (NAFLD). The underlying mechanism of hepatic injury in these models, and how this reflects human disease remains incompletely understood. We used detailed transcriptional analysis to interrogate the molecular mechanisms of this intervention and its similarity to human disease. Adult C57Bl/6J mice were maintained on control, choline deficient (CDD) or methionine/choline deficient (MCDD) diets for 4 weeks. Isolated liver RNA was used for transcriptional profiling by micro array analysis.

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Effect of methionine/choline deficient diet on liver and suprachiasmatic nucleus circadian transcriptome.

Project description:The feeding/fasting cycles controlled by our circadian clock impose great daily metabolic and physiological changes, and yet investigations into the consequences of metabolic deficiencies, either dietary or genetic, have often ignored the time of day or the circadian time of the animals or subjects. In addition, these deficiencies may themselves disrupt our circadian clock, causing secondary metabolic, physiological and behavioural disorders. Dietary methionine/choline deficiency in rodents is a common model for human non-alcoholic steatohepatitis, but methionine and choline are nutrients essential for many other processes beyond fatty acid synthesis in the liver, including biological methylations and 1-carbon metabolism, regulation of translation notably via the mTOR pathway, phospholipid synthesis, polyamine pathway and glutathione synthesis. We have previously shown that circadian rhythms in many organisms are highly sensitive to deficiency or excesses of 1-carbon metabolites. Using a methionine/choline deficient diet in mice, we illustrate the nutrigenomic crosstalk between circadian rhythms and 1-carbon metabolism. We show not only that circadian locomotor activity behaviour is profoundly, rapidly and reversibly affected by methionine/choline deficiency, but also that the effects of methionine/choline deficiency on gene expression and 1-carbon metabolites are dependent on circadian time, illustrating the importance of considering circadian rhythms in metabolic studies. This study also highlights the impact of what we eat, or don't, on our behaviour and biological rhythms.

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Project description:Choline supplies methyl groups for regeneration of methionine and the methyl donor S-adenosylmethionine in the liver. Here we demonstrate that the catabolism of membrane phosphatidylcholine (PC) into water-soluble glycerophosphocholine (GPC) by the phospholipase/lysophospholipase PNPLA8-PNPLA7 axis enables endogenous choline stored in hepatic PC to be utilized in methyl metabolism. PNPLA7-deficient mice show marked decreases in hepatic GPC, choline, and several metabolites related to the methionine cycle, accompanied by various signs of methionine insufficiency including growth retardation, hypoglycemia, hypolipidemia, increased energy consumption, reduced adiposity, increased FGF21, and an altered epigenetic methylation landscape. Moreover, PNPLA8-deficient mice recapitulate most of these phenotypes. In contrast to wild-type mice fed a methionine/choline-deficient diet, both knockout strains display a decreased hepatic triglyceride likely via reductions of lipogenesis and GPC-derived glycerol flux. Collectively, our findings highlight the biological importance of phospholipid catabolism driven by PNPLA8/PNPLA7 in methyl group flux and triglyceride synthesis in the liver.

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