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PPARa regulates ER-lipid droplet protein Calsyntenin-3b to promote ketogenesis in hepatocytes

ABSTRACT: PPARa regulates ER-lipid droplet protein Calsyntenin-3b to promote ketogenesis in hepatocytes

PROVIDER: PRJNA1224734 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32367931_1.fastq.gz	Fastqsanger.gz
	SRR32367931_2.fastq.gz	Fastqsanger.gz
	SRR32367932_1.fastq.gz	Fastqsanger.gz
	SRR32367932_2.fastq.gz	Fastqsanger.gz
	SRR32367933_1.fastq.gz	Fastqsanger.gz

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PPARa regulates ER-lipid droplet protein Calsyntenin-3b to promote ketogenesis in hepatocytes

Project description:Ketogenesis requires fatty acid flux from intrahepatic (lipid droplets) and extrahepatic (adipose tissue) lipid stores to hepatocyte mitochondria. However, whether inter-organelle contact sites regulate this process is unknown. Recent studies have revealed a role for Calsyntenin-3b (CLSTN3b), an endoplasmic reticulum-lipid droplet contact site protein, in the control of lipid utilization in adipose tissue. Here, we show that Clstn3b expression is induced in the liver by the nuclear receptor PPARa in settings of high lipid utilization, including fasting and ketogenic diet feeding. Hepatocyte-specific loss of CLSTN3b in mice impairs ketogenesis independent of changes in PPARa activation. Conversely, hepatic overexpression of CLSTN3b promotes ketogenesis in mice. Mechanistically, CLSTN3b affects LD-mitochondria crosstalk, as evidenced by changes in fatty acid oxidation, lipolysis-dependent mitochondrial respiration, and the mitochondrial integrated stress response. These findings define a function for CLSTN3b-dependent membrane contacts in hepatic lipid utilization and ketogenesis.

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Project description:Like many per- or polyfluorinated alkyl substances (PFAS), toxicity studies with HFPO-DA (ammonium, 2,3,3,3-tetrafluoro-2-(heptafluoropropoxy)-propanoate; CASRN 62037-80-3), a short-chain PFAS used in the manufacture of some types of fluorinated polymers, indicate that the liver is the primary target of toxicity in rodents following oral exposure. Although the current weight of evidence supports the PPARa mode of action (MOA) for liver effects in HFPO-DA-exposed mice, alternate MOAs have also been hypothesized including PPARg or cytotoxicity. To further evaluate the MOA for HFPO-DA in rodent liver, transcriptomic analyses were conducted on samples from primary mouse, rat and pooled human hepatocytes treated for 12, 24 or 72 hours with various concentrations of HFPO-DA, or established agonists of PPARa (GW7647), PPARg (rosiglitazone), or cytotoxic agents (i.e., acetaminophen or d-galactosamine). Concordance analyses of enriched pathways across chemicals within each species demonstrated greatest concordance between HFPO-DA and PPARa agonist GW7647-treated hepatocytes compared to the other chemicals evaluated. These findings were supported by benchmark concentration modeling and predicted upstream regulator results. In addition, transcriptomic analyses across species demonstrated a greater transcriptomic response in rodent hepatocytes treated with HFPO-DA or agonists of PPARa or PPARg, indicating rodent hepatocytes are more sensitive to HFPO-DA or PPARa/g agonist treatment. These results are consistent with previously published transcriptomic analyses and further support that liver effects in HFPO-DA-exposed rodents are mediated through rodent-specific PPARa signaling mechanisms as part of the MOA for PPARa activator-induced rodent hepatocarcinogenesis.

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