ArticleMetabolism open2021
Deficiency of SREBP1c modulates autophagy mediated lipid droplet catabolism during oleic acid induced steatosis.
Article in Metabolism open, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Adipose Tissue Immunosuppressive T Cells Regulate Atherosclerosis Development and Liver Fat Accumulation in Obesity.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- The Role of FGF1 in Chronic Liver Diseases.Biomedicines · 2026Review
- Metabolic Dysfunction-Associated Steatotic Liver Disease and Emerging Oligonucleotide Therapies.International journal of biological sciences · 2026Review
- Metabolic-Dysfunction-Associated Steatotic Liver Disease: Molecular Mechanisms, Clinical Implications, and Emerging Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Favorable inhibitory effect of clodronate on hepatic steatosis in short bowel syndrome model rats.Pediatric surgery international · 2024Article
- Uridine diphosphate glucuronosyltransferase 1A1 prevents the progression of liver injury.World journal of gastroenterology · 2024Article
- Editorial: Special issue: Non-alcoholic fatty liver disease: From molecular basis to therapeutic advances.Metabolism open · 2023Article
- Multiomics Approach Captures Hepatic Metabolic Network Altered by Chronic Ethanol Administration.Biology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIncreased fatty acid and triglyceride synthesis in liver, majorly modulated by Sterol Regulator Elementing Binding Protein 1c (SREBP1c), is one of the main features of non-alcoholic fatty liver disease (NAFLD). In the present study, we aimed to identify the relation between SREBP1c and autophagy mediated lipid droplet (LD) catabolism in oleic acid (OA) induced lipid accumulation.
methodsIncreased LD formation and SREBP1c induction were identified in hepatocytes (AML12 cells) following the OA administration. SREBP1c level was reduced through siRNA against SREBP1c. The amount and the size of LDs were determined by BODIPY, while protein and mRNA expressions were identified by immunoblotting and qRT-PCR, respectively. LD-lysosome colocalization was determined with immunofluorescence.
resultsIncreased LD formation and SREBP1c levels were determined at 0.06 mM OA concentration. SREBP1c silencing reduced the number of LDs, while increasing mRNA levels of PPARα. On the other hand, SREBP1c silencing in non-OA and OA treated cells enhanced autophagy mediated LD catabolism.
conclusionOur results implicate the effect of SREBP1c deficiency in modulating PPARα signaling and autophagy mediated LD catabolism against OA induced lipid accumulation.
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