ArticleThe Journal of biological chemistry2015
RGC-32 Deficiency Protects against Hepatic Steatosis by Reducing Lipogenesis.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Diclofenac Disrupts the Circadian Clock and through Complex Cross-Talks Aggravates Immune-Mediated Liver Injury-A Repeated Dose Study in Minipigs for 28 Days.International journal of molecular sciences · 2023Article
- Regulator of Cell Cycle Protein (RGCC/RGC-32) Protects against Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Anlotinib Downregulates RGC32 Which Provoked by Bevacizumab.Frontiers in oncology · 2022Article
- ADAR1 deficiency protects against high-fat diet-induced obesity and insulin resistance in mice.American journal of physiology. Endocrinology and metabolism · 2021Article
- From cirrhosis to hepatocellular carcinoma: An investigation into hepatitis C viral oncogenesis.Hepatology forum · 2020Article
- RGC-32 and diseases: the first 20 years.Immunologic research · 2019Review
- Loss of Response Gene to Complement 32 (RGC-32) in Diabetic Mouse Retina Is Involved in Retinopathy Development.International journal of molecular sciences · 2018Article
- Response Gene to Complement 32 Maintains Blood Pressure Homeostasis by Regulating α-Adrenergic Receptor Expression.Circulation research · 2018Article
- Response gene to complement 32 suppresses adipose tissue thermogenic genes through inhibiting β3-adrenergic receptor/mTORC1 signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- New insights into the roles of RGC-32.Cellular & molecular immunology · 2018Article
- RGC-32 (Response Gene to Complement 32) Deficiency Protects Endothelial Cells From Inflammation and Attenuates Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Response Gene to Complement 32 in Vascular Diseases.Frontiers in cardiovascular medicine · 2018Review
- RGC32 induces epithelial-mesenchymal transition by activating the Smad/Sip1 signaling pathway in CRC.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Hepatic steatosis is associated with insulin resistance and metabolic syndrome because of increased hepatic triglyceride content. We have reported previously that deficiency of response gene to complement 32 (RGC-32) prevents high-fat diet (HFD)-induced obesity and insulin resistance in mice. This study was conducted to determine the role of RGC-32 in the regulation of hepatic steatosis. We observed that hepatic RGC-32 was induced dramatically by both HFD challenge and ethanol administration. RGC-32 knockout (RGC32(-/-)) mice were resistant to HFD- and ethanol-induced hepatic steatosis. The hepatic triglyceride content of RGC32(-/-) mice was decreased significantly compared with WT controls even under normal chow conditions. Moreover, RGC-32 deficiency decreased the expression of lipogenesis-related genes, sterol regulatory element binding protein 1c (SREBP-1c), fatty acid synthase, and stearoyl-CoA desaturase 1 (SCD1). RGC-32 deficiency also decreased SCD1 activity, as indicated by decreased desaturase indices of the liver and serum. Mechanistically, insulin and ethanol induced RGC-32 expression through the NF-κB signaling pathway, which, in turn, increased SCD1 expression in a SREBP-1c-dependent manner. RGC-32 also promoted SREBP-1c expression through activating liver X receptor. These results demonstrate that RGC-32 contributes to the development of hepatic steatosis by facilitating de novo lipogenesis through activating liver X receptor, leading to the induction of SREBP-1c and its target genes. Therefore, RGC-32 may be a potential novel drug target for the treatment of hepatic steatosis and its related diseases.
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