Oleic Acid Promotes Lipid Accumulation in Bovine Adipocytes: The Role of PPARα Activity
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1168535 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30874617_1.fastq.gz | Fastqsanger.gz | |||
| SRR30874617_2.fastq.gz | Fastqsanger.gz | |||
| SRR30874618_1.fastq.gz | Fastqsanger.gz | |||
| SRR30874618_2.fastq.gz | Fastqsanger.gz | |||
| SRR30874619_1.fastq.gz | Fastqsanger.gz |
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Project description:Sesamin alleviates lipid accumulation induced by oleic acid in HepG2 cells
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Project description:Sesamin, a special compound present in sesame and sesame oil, has been reported the role in regulating blood lipids and improving liver function, while the underlying mechanisms remain unclear. This study aims to explore its potential mechanisms in regulating lipid metabolism. HepG2 cells were treated with oleic acid to establish an in vitro high-fat cell model to simulate impaired hepatocytes under lipid metabolism disorders.Differentially expressed genes during the sesame intervention were screened by RNA sequencing (RNA seq) and validated using real-time quantitative PCR and Western blot.The data showed that sesamin significantly upregulated the mRNA levels of genes involved in fatty acid metabolism processes such as ETFB, ACAT2, FADS2, FABP1, ACOT1, and those involved in cholesterol metabolism processes such as FDPS, PCSK9, and DHCR7, and downregulated the mRNA levels of CYP24A1 and GGT5 involved in fatty acid metabolism, as well as MVK involved in cholesterol synthesis. Sesamin significantly down-regulated the protein levels of NOTCH1, CD36, SOX4, and FABP1. In summary, sesamin alleviates lipid accumulation in HepG2 by regulating lipid metabolism, with potential mechanisms involving steroid biosynthesis, unsaturated fatty acid biosynthesis, fat digestion and absorption, fatty acid metabolism, Notch signaling pathway, and PPAR signaling pathway.
2023-12-05 | GSE248903 | GEO
Project description:Objective : This work aimed at characterizing PPARα involvement in metabolism regulation and at comparing PPARα and PPARγ roles in human white adipocytes. Research Design and Methods : Profiling of gene expression alterations was assessed with microarrays and RT-qPCR. Primary cultures of human adipocytes were treated with PPARα agonist GW7647 or PPARγ agonist Rosiglitazone. Western blot were used to determine protein level modifications. Metabolic changes were evaluated with palmitate and glucose oxidation studies and with metabolite measurements. Results : GW7647 induces an upregulation of β-oxidation gene expression and increases palmitate oxidation. Unexpectedly glycolysis was strongly reduced at transcriptional and functional levels by GW7647 while the overall glucose oxidation remains unaltered, leading to a decrease in pyruvate and lactate production. Moreover lipogenesis was downregulated by GW7647 inhibiting triglyceride esterification and de novo lipogenesis. GW7647 induced alterations were abolished by a PPARα antagonist treatment and were clearly different from Rosiglitazone effects. Rosiglitazone had no major impact on glycolysis and β-oxidation but increased glucose incorporation into glycerol backbone of triglycerides. Conclusions : Altogether these results show that PPARα can upregulate β-oxidation in human white adipocytes. Its pharmacological activation may be used to oxidize fatty acids in situ when lipolysis is activated thus preventing their release into systemic circulation. We treated four adipocyte cultures, each one coming from different subjects, with GW7647, Rosiglitazone (ROSI) or DMSO. DMSO treated cells are control samples. Thus we have four paired sample groups for each treatment (GW7647 and ROSI).
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Project description:An overload of hepatic fatty acids, such as oleic acid is a key trigger of non-alcoholic fatty liver disease (NAFLD). Here, we investigated whether Artemisia frigida, a valuable traditional medicine used to treat various diseases, could mitigate OA-induced lipid accumulation in HepG2 cells. Then, to identify the active substances in A. frigida, a phytochemistry investigation was conducted using a bioassay-guided isolation method. Consequently, one terpene (1) and one flavone (2) were identified. Compound 1 ((+)-dehydrovomifoliol) exhibited potent effects against lipid accumulation in OA-induced HepG2 cells, without causing cyto-toxicity. Notably, treatment with (+)-dehydrovomifoliol decreased the expression levels of three genes related to lipogenesis (SREBP1, ACC, and FASN) and increased those of three genes related to fatty acid oxidation (PPARα, ACOX1, and FGF21). In addition, similar results were observed for SREBP1, PPARα, and FGF21 protein levels. The effects of (+)-dehydrovomifoliol were partially reversed by treatment with the PPARα antagonist GW6471, indicating the important role of the PPARα-FGF21 axis in the effects of (+)-dehydrovomifoliol. Based on its effects on hepatic lipogenesis and fatty acid oxidation signaling via the PPARα-FGF21 axis, (+)-dehydrovomifoliol isolated from A. frigida could be a useful early lead compound for developing new drugs for NAFLD prevention.
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Project description:Autophagy is an evolutionally conserved catabolic process that recycles nutrients upon starvation and maintains cellular energy homeostasis1-3. Its acute regulation by nutrient sensing signaling pathways is well described, but its longer-term transcriptional regulation is not. The nuclear receptors PPARα and FXR are activated in the fasted or fed liver, respectively4,5. Here we show that both regulate hepatic autophagy. Pharmacologic activation of PPARα reverses the normal suppression of autophagy in the fed state, inducing autophagic lipid degradation, or lipophagy. This response is lost in PPARα knockout (PPARα-/-) mice, which are partially defective in the induction of autophagy by fasting. Pharmacologic activation of the bile acid receptor FXR strongly suppresses the induction of autophagy in the fasting state, and this response is absent in FXR knockout (FXR-/-) mice, which show a partial defect in suppression of hepatic autophagy in the fed state. PPARα and FXR compete for binding to shared sites in autophagic gene promoters, with opposite transcriptional outputs. These results reveal complementary, interlocking mechanisms for regulation of autophagy by nutrient status. Mouse liver PPARα cistromes in fed 8-week-old male WT or PPARα KO mice treated with or without its synthetic agonist ligand GW7647twice a day were generated by deep sequencing in quadruplicate using illumina
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Project description:Compared to ordinary rapeseed, high-oleic acid rapeseed has higher levels of monounsaturated fatty acids and lower levels of saturated fatty acid and polyunsaturated fatty acids, and thus is of high nutritional and health value. In addition, high-oleic acid rapeseed oil imparts cardiovascular protective effects. Based on these properties, high-oleic acid oil crops have been extensively investigated and cultivated. In this study, we employed a microarray analysis with high oleic acid line and low oleic acid line from the developing seeds (27 days after flowering) of Brassica napus.
2018-09-20 | GSE120223 | GEO
Project description:Objective : This work aimed at characterizing PPARα involvement in metabolism regulation and at comparing PPARα and PPARγ roles in human white adipocytes. Research Design and Methods : Profiling of gene expression alterations was assessed with microarrays and RT-qPCR. Primary cultures of human adipocytes were treated with PPARα agonist GW7647 or PPARγ agonist Rosiglitazone. Western blot were used to determine protein level modifications. Metabolic changes were evaluated with palmitate and glucose oxidation studies and with metabolite measurements. Results : GW7647 induces an upregulation of β-oxidation gene expression and increases palmitate oxidation. Unexpectedly glycolysis was strongly reduced at transcriptional and functional levels by GW7647 while the overall glucose oxidation remains unaltered, leading to a decrease in pyruvate and lactate production. Moreover lipogenesis was downregulated by GW7647 inhibiting triglyceride esterification and de novo lipogenesis. GW7647 induced alterations were abolished by a PPARα antagonist treatment and were clearly different from Rosiglitazone effects. Rosiglitazone had no major impact on glycolysis and β-oxidation but increased glucose incorporation into glycerol backbone of triglycerides. Conclusions : Altogether these results show that PPARα can upregulate β-oxidation in human white adipocytes. Its pharmacological activation may be used to oxidize fatty acids in situ when lipolysis is activated thus preventing their release into systemic circulation.
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Project description:The class 3 phosphoinositide 3-kinase (PI3K) is required for the lysosomal degradation by autophagy and vesicular trafficking, assuring adaptation to energy shortages. Mitochondrial lipid catabolism is another important energy source. Autophagy and mitochondrial metabolism are transcriptionally controlled by nutrient sensing nuclear receptors. However, it is not known whether the class 3 PI3K contributes to this regulation. Here we show that hepatocyte-specific inactivation of Vps15, the essential regulatory subunit of the class 3 PI3K, results in mitochondrial depletion and a failure to oxidize fatty acids. Mechanistically, the transcriptional activity of Peroxisome Proliferator Activated Receptor alpha (PPARα), a nuclear receptor that orchestrates fatty acid catabolism, is blunted in Vps15-deficient livers. We find PPARα transcriptional repressors Histone Deacetylase 3 (Hdac3) and Nuclear receptor co-repressor 1 (NCoR1) accumulated in Vps15-deficient livers due to defective autophagic flux. Pharmacologic activation of PPARα with a synthetic ligand, re-expression of its co-activator Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha (PGC-1α) or inhibition of Hdac3 restored mitochondrial biogenesis and lipid oxidation in Vps15-deficient hepatocytes. These findings reveal a role for the class 3 PI3K and autophagy in transcriptional coordination of mitochondrial metabolism.
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