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Mtfp1 ablation enhances mitochondrial respiration and protects against hepatic steatosis

ABSTRACT: Mtfp1 ablation enhances mitochondrial respiration and protects against hepatic steatosis

PROVIDER: PRJEB61894 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR11403700_1.fastq.gz	Fastqsanger.gz
	ERR11403700_2.fastq.gz	Fastqsanger.gz
	ERR11403701_1.fastq.gz	Fastqsanger.gz
	ERR11403701_2.fastq.gz	Fastqsanger.gz
	ERR11403702_1.fastq.gz	Fastqsanger.gz

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Mtfp1 ablation enhances respiration and protects against hepatic steatosis

Project description:Hepatic steatosis is the result of an imbalance between nutrient delivery and metabolism in the liver. It is the first hallmark of Non-alcoholic fatty liver disease (NAFLD) and is characterized by the accumulation of excess lipids in the liver that can drive liver failure, inflammation, and cancer. Mitochondria control the fate and function of cells and compelling evidence implicates these multifunctional organelles in the appearance and progression of liver dysfunction, although it remains to be elucidated which specific mitochondrial functions are actually causally linked to NAFLD. In this study, we identified Mitochondrial Fission Process 1 protein (MTFP1) as a key regulator of mitochondrial and metabolic activity in the liver. Deletion of Mtfp1 in hepatocytes is physiologically benign in mice yet leads to the upregulation of oxidative phosphorylation (OXPHOS) complexes and mitochondrial respiration, independently of mitochondrial biogenesis. Consequently, hepatocyte-specific knockout mice are protected against high fat diet-induced hepatic steatosis and metabolic dysregulation. Additionally, we find that deletion of Mtfp1 in liver mitochondria inhibits mitochondrial permeability transition pore opening in hepatocytes, conferring protection against apoptotic liver damage in vivo and ex vivo. Our work uncovers novel functions of MTFP1 in the liver, positioning this gene as an unexpected regulator of OXPHOS and a therapeutic candidate for NAFLD.

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Mtfp1 ablation enhances mitochondrial respiration and protects against hepatic steatosis

Project description:The present study identified the role of the Mitochondrial Fission Process 1 protein (MTFP1) in the mitochondrial and metabolic activity of the liver. Ablation of Mtfp1 liver cells alters mitochondrial function and confers a specific liver metabolic protection against high-fat diet

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Mtfp1 ablation enhances mitochondrial respiration and protects against hepatic steatosis- Co-IP

Project description:Hepatic steatosis is the result of an imbalance between nutrient delivery and metabolism in the liver. It is the first hallmark of Non-alcoholic fatty liver disease (NAFLD) and is characterized by the accumulation of excess lipids in the liver that can drive liver failure, inflammation, and cancer. Mitochondria control the fate and function of cells and compelling evidence implicates these multifunctional organelles in the appearance and progression of liver dysfunction, although it remains to be elucidated which specific mitochondrial functions are actually causally linked to NAFLD. Here, we identified Mitochondrial Fission Process 1 protein (MTFP1) as a key regulator of mitochondrial and metabolic activity in the liver. Deletion of Mtfp1 in hepatocytes is physiologically benign in mice yet leads to the upregulation of oxidative phosphorylation (OXPHOS) complexes and mitochondrial respiration, independently of mitochondrial biogenesis. Consequently, hepatocyte-specific knockout mice are protected against high fat diet-induced hepatic steatosis and metabolic dysregulation. Additionally, we find that deletion of Mtfp1 in liver mitochondria inhibits mitochondrial permeability transition pore opening in hepatocytes, conferring protection against apoptotic liver damage in vivo and ex vivo. Our work uncovers novel functions of MTFP1 in the liver, positioning this gene as an unexpected regulator of OXPHOS and a therapeutic candidate for NAFLD.

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Removing a Double Bond from Ceramides Ameliorates Insulin Resistance and Hepatic Steatosis

Project description:Ceramides contribute to the lipotoxicity that underlies diabetes, hepatic steatosis, and heart disease. By genetically engineering mice, we deleted the enzyme dihydroceramide desaturase-1 (DES1) which inserts a conserved double bond into the backbone of ceramides and other predominant sphingolipids. Ablation of DES1 from whole animals, or tissue-specific deletion in the liver, and/or adipose tissue resolved hepatic steatosis and insulin resistance in mice caused by leptin deficiency or obesogenic diets. Mechanistic studies revealed new ceramide actions that promoted lipid uptake and storage and impaired glucose utilization, none of which could be recapitulated by (dihydro)ceramides that lacked the critical double bond. These studies suggest that inhibition of DES1 may provide a means of treating hepatic steatosis and cardiometabolic disorders.

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Resolvin D2-GPR18 Enhances Bone Marrow Function and Limits Steatosis and Hepatic Collagen Accumulation in Aging

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