The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Loss of progesterone receptor membrane component 1 promotes hepatic steatosis via the induced de novo lipogenesis
Abstract
Non-alcoholic fatty liver disease (NAFLD) results from triglyceride accumulation within the liver and some of them advances to non-alcoholic steatohepatitis (NASH). It is important to note that in NAFLD development, hepatic de novo lipogenesis (DNL) derives from excess carbohydrates and fats under a condition of excess energy through β-oxidation. As a main regulator for DNL, sterol regulatory element-binding protein 1 (Srebp-1) forms complex with progesterone receptor membrane component 1 (Pgrmc1). To investigate whether Pgrmc1 may have a notable effect on DNL via SREBP-1 activation, we generated Pgrmc1 knockout (KO) mice and fed a high fat diet for one month. High-fat-fed Pgrmc1 KO mice showed a substantial increase in levels of hepatic TG accumulation, and they were predisposed to NAFLD when compared to WT mice. Loss of Pgrmc1 increased mature SREBP-1 protein level, suggesting that induction of hepatic steatosis in Pgrmc1 KO mice might be triggered by de novo lipogenesis. Moreover, Pgrmc1 KO mice were also more vulnerable to early stage of NASH, showing high levels of alanine aminotransferase, obesity-linked pro-inflammatory cytokines, and fibrosis markers. This is interesting because Pgrmc1 involves with the first step in regulating the hepatic de novo lipogenesis under an excess energy condition.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
TMEM97 levels can be regulated by changes in cholesterol levels; when cholesterol levels are reduced, TMEM97 expression can be induced by sterol regulatory element-binding protein-2.
“Although TMEM97, unlike emopamil binding protein, is not thought to have isomerase activity, TMEM97 levels can be regulated by changes in cholesterol levels. More specifically, when cholesterol levels are reduced, TMEM97 expression can be induced by sterol regulatory element-binding protein-2 [75,76,77,78].”
From Sigma-2 Receptors—From Basic Biology to Therapeutic Target: A Focus on Age-Related Degenerative Diseases (2023) · cites this paper as [76]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Lambert, J. E., Ramos–Roman, M. A., Browning, J. D., & Parks, E. J. (2014) · Gastroenterology · doi:10.1053/j.gastro.2013.11.049 · Cited by 1,069
Schwarz, J.-M., Linfoot, P., Dare, D., & Aghajanian, K. (2003) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/77.1.43 · Cited by 496
Yang, L., Roh, Y. S., Song, J., Zhang, B., Liu, C., Loomba, R., & Seki, E. (2014) · Hepatology · doi:10.1002/hep.26698 · Cited by 275
A Potential Mechanism Underlying Atypical Antipsychotics-Induced Lipid Disturbances
Cai, H. L., Tan, Q. Y., Jiang, P., Dang, R. L., Xue, Y., Tang, M. M., Xu, P., Deng, Y., Li, H. D., & Yao, J. K. (2015) · Translational Psychiatry · doi:10.1038/tp.2015.161 · Cited by 86
Flagged first, then by citations
Research works printed but not linked: 46
- Chalasani, N. et al. The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. Gastroenterology 142, 1592–1609, https://doi.org/10.1053/j.gastro.2012.04.001 (2012). · DOI
- Tarantino, G., Savastano, S. & Colao, A. Hepatic steatosis, low-grade chronic inflammation and hormone/growth factor/adipokine imbalance. World J Gastroenterol 16, 4773–4783 (2010). · DOI
- Starley, B. Q., Calcagno, C. J. & Harrison, S. A. Nonalcoholic fatty liver disease and hepatocellular carcinoma: a weighty connection. Hepatology 51, 1820–1832, https://doi.org/10.1002/hep.23594 (2010). · DOI
- Tarantino, G. & Finelli, C. What about non-alcoholic fatty liver disease as a new criterion to define metabolic syndrome? World J Gastroenterol 19, 3375–3384, https://doi.org/10.3748/wjg.v19.i22.3375 (2013). · DOI
- Buzzetti, E., Pinzani, M. & Tsochatzis, E. A. The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). Metabolism 65, 1038–1048, https://doi.org/10.1016/j.metabol.2015.12.012 (2016). · DOI · Paper page
- Onnerhag, K., Nilsson, P. M. & Lindgren, S. Increased risk of cirrhosis and hepatocellular cancer during long-term follow-up of patients with biopsy-proven NAFLD. Scand J Gastroenterol 49, 1111–1118, https://doi.org/10.3109/00365521.2014.934911 (2014). · DOI
- Shimano, H. et al. Isoform 1c of sterol regulatory element binding protein is less active than isoform 1a in livers of transgenic mice and in cultured cells. J Clin Invest 99, 846–854, https://doi.org/10.1172/JCI119248 (1997). · DOI · Paper page
- Horton, J. D., Goldstein, J. L. & Brown, M. S. SREBPs: activators of the complete program of cholesterol and fatty acid synthesis in the liver. J Clin Invest 109, 1125–1131, https://doi.org/10.1172/JCI15593 (2002). · DOI · Paper page
- Hagen, R. M., Rodriguez-Cuenca, S. & Vidal-Puig, A. An allostatic control of membrane lipid composition by SREBP1. FEBS Lett 584, 2689–2698, https://doi.org/10.1016/j.febslet.2010.04.004 (2010). · DOI
- Kast-Woelbern, H. R. et al. Rosiglitazone induction of Insig-1 in white adipose tissue reveals a novel interplay of peroxisome proliferator-activated receptor gamma and sterol regulatory element-binding protein in the regulation of adipogenesis. J Biol Chem 279, 23908–23915, https://doi.org/10.1074/jbc.M403145200 (2004). · DOI
- Shulman, A. I. & Mangelsdorf, D. J. Retinoid x receptor heterodimers in the metabolic syndrome. N Engl J Med 353, 604–615, https://doi.org/10.1056/NEJMra043590 (2005). · DOI
- Tobin, K. A. et al. Cross-talk between fatty acid and cholesterol metabolism mediated by liver X receptor-alpha. Mol Endocrinol 14, 741–752, https://doi.org/10.1210/mend.14.5.0459 (2000). · DOI
- Yoshikawa, T. et al. Cross-talk between peroxisome proliferator-activated receptor (PPAR) alpha and liver X receptor (LXR) in nutritional regulation of fatty acid metabolism. I. PPARs suppress sterol regulatory element binding protein-1c promoter through inhibition of LXR signaling. Mol Endocrinol 17, 1240–1254, https://doi.org/10.1210/me.2002-0190 (2003). · DOI
- Matsuda, M. et al. SREBP cleavage-activating protein (SCAP) is required for increased lipid synthesis in liver induced by cholesterol deprivation and insulin elevation. Genes Dev 15, 1206–1216, https://doi.org/10.1101/gad.891301 (2001). · DOI · Paper page
- Liu, F. H. et al. The gene-gene interaction of INSIG-SCAP-SREBP pathway on the risk of obesity in Chinese children. Biomed Res Int 2014, 538564, https://doi.org/10.1155/2014/538564 (2014). · DOI
- Dong, X. Y. & Tang, S. Q. Insulin-induced gene: a new regulator in lipid metabolism. Peptides 31, 2145–2150, https://doi.org/10.1016/j.peptides.2010.07.020 (2010). · DOI
- Suchanek, M., Radzikowska, A. & Thiele, C. Photo-leucine and photo-methionine allow identification of protein-protein interactions in living cells. Nat Methods 2, 261–267, https://doi.org/10.1038/nmeth752 (2005). · DOI
- Krebs, C. J. et al. A membrane-associated progesterone-binding protein, 25-Dx, is regulated by progesterone in brain regions involved in female reproductive behaviors. Proc Natl Acad Sci USA 97, 12816–12821, https://doi.org/10.1073/pnas.97.23.12816 (2000). · DOI
- Selmin, O. et al. Isolation and characterization of a novel gene induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat liver. Carcinogenesis 17, 2609–2615 (1996). · DOI
- Zhang, M. et al. Progesterone receptor membrane component 1 is a functional part of the glucagon-like peptide-1 (GLP-1) receptor complex in pancreatic beta cells. Mol Cell Proteomics 13, 3049–3062, https://doi.org/10.1074/mcp.M114.040196 (2014). · DOI
- Peluso, J. J., Romak, J. & Liu, X. Progesterone receptor membrane component-1 (PGRMC1) is the mediator of progesterone’s antiapoptotic action in spontaneously immortalized granulosa cells as revealed by PGRMC1 small interfering ribonucleic acid treatment and functional analysis of PGRMC1 mutations. Endocrinology 149, 534–543, https://doi.org/10.1210/en.2007-1050 (2008). · DOI
- Rohe, H. J., Ahmed, I. S., Twist, K. E. & Craven, R. J. PGRMC1 (progesterone receptor membrane component 1): a targetable protein with multiple functions in steroid signaling, P450 activation and drug binding. Pharmacol Ther 121, 14–19, https://doi.org/10.1016/j.pharmthera.2008.09.006 (2009). · DOI · Paper page
- Hughes, A. L. et al. Dap1/PGRMC1 binds and regulates cytochrome P450 enzymes. Cell Metab 5, 143–149, https://doi.org/10.1016/j.cmet.2006.12.009 (2007). · DOI · Paper page
- Satapati, S. et al. Mitochondrial metabolism mediates oxidative stress and inflammation in fatty liver. J Clin Invest 125, 4447–4462, https://doi.org/10.1172/JCI82204 (2015). · DOI
- Fabbrini, E., Sullivan, S. & Klein, S. Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications. Hepatology 51, 679–689, https://doi.org/10.1002/hep.23280 (2010). · DOI · Paper page
- Farrell, G. C. & Larter, C. Z. Nonalcoholic fatty liver disease: from steatosis to cirrhosis. Hepatology 43, S99–S112, https://doi.org/10.1002/hep.20973 (2006). · DOI
- Caldwell, S. H., Crespo, D. M., Kang, H. S. & Al-Osaimi, A. M. Obesity and hepatocellular carcinoma. Gastroenterology 127, S97–103 (2004). · DOI
- Xu, X., So, J. S., Park, J. G. & Lee, A. H. Transcriptional control of hepatic lipid metabolism by SREBP and ChREBP. Semin Liver Dis 33, 301–311, https://doi.org/10.1055/s-0033-1358523 (2013). · DOI
- Rawson, R. B. The SREBP pathway–insights from Insigs and insects. Nat Rev Mol Cell Biol 4, 631–640, https://doi.org/10.1038/nrm1174 (2003). · DOI · Paper page
- Li, X. et al. SREBP-1c overexpression induces triglycerides accumulation through increasing lipid synthesis and decreasing lipid oxidation and VLDL assembly in bovine hepatocytes. J Steroid Biochem Mol Biol 143, 174–182, https://doi.org/10.1016/j.jsbmb.2014.02.009 (2014). · DOI
- Mao, J. et al. Liver-specific deletion of acetyl-CoA carboxylase 1 reduces hepatic triglyceride accumulation without affecting glucose homeostasis. Proc Natl Acad Sci USA 103, 8552–8557, https://doi.org/10.1073/pnas.0603115103 (2006). · DOI · Paper page
- Sun, Y. et al. SREBP1 regulates tumorigenesis and prognosis of pancreatic cancer through targeting lipid metabolism. Tumour Biol 36, 4133–4141, https://doi.org/10.1007/s13277-015-3047-5 (2015). · DOI
- Zhang, H. et al. Differential effects of estrogen/androgen on the prevention of nonalcoholic fatty liver disease in the male rat. J Lipid Res 54, 345–357, https://doi.org/10.1194/jlr.M028969 (2013). · DOI
- Brookheart, R. T., Michel, C. I. & Schaffer, J. E. As a matter of fat. Cell Metab 10, 9–12, https://doi.org/10.1016/j.cmet.2009.03.011 (2009). · DOI · Paper page
- Li, Z. Z., Berk, M., McIntyre, T. M. & Feldstein, A. E. Hepatic lipid partitioning and liver damage in nonalcoholic fatty liver disease: role of stearoyl-CoA desaturase. J Biol Chem 284, 5637–5644, https://doi.org/10.1074/jbc.M807616200 (2009). · DOI
- Peter, A. et al. Individual stearoyl-coa desaturase 1 expression modulates endoplasmic reticulum stress and inflammation in human myotubes and is associated with skeletal muscle lipid storage and insulin sensitivity in vivo. Diabetes 58, 1757–1765, https://doi.org/10.2337/db09-0188 (2009). · DOI
- Verma, S., Jensen, D., Hart, J. & Mohanty, S. R. Predictive value of ALT levels for non-alcoholic steatohepatitis (NASH) and advanced fibrosis in non-alcoholic fatty liver disease (NAFLD). Liver Int 33, 1398–1405, https://doi.org/10.1111/liv.12226 (2013). · DOI
- Hotamisligil, G. S. Inflammation and metabolic disorders. Nature 444, 860–867, https://doi.org/10.1038/nature05485 (2006). · DOI · Paper page
- Park, E. J. et al. Dietary and genetic obesity promote liver inflammation and tumorigenesis by enhancing IL-6 and TNF expression. Cell 140, 197–208, https://doi.org/10.1016/j.cell.2009.12.052 (2010). · DOI · Paper page
- Tarantino, G. et al. Could inflammatory markers help diagnose nonalcoholic steatohepatitis? European journal of gastroenterology & hepatology 21, 504–511, https://doi.org/10.1097/MEG.0b013e3283229b40 (2009). · DOI
- Matsumoto, M. et al. An improved mouse model that rapidly develops fibrosis in non-alcoholic steatohepatitis. Int J Exp Pathol 94, 93–103, https://doi.org/10.1111/iep.12008 (2013). · DOI · Paper page
- Lee, N. P. et al. Proteomic expression signature distinguishes cancerous and nonmalignant tissues in hepatocellular carcinoma. J Proteome Res 8, 1293–1303, https://doi.org/10.1021/pr800637z (2009). · DOI
- Hampton, K. K., Stewart, R., Napier, D., Claudio, P. P. & Craven, R. J. PGRMC1 Elevation in Multiple Cancers and Essential Role in Stem Cell Survival. Adv Lung Cancer (Irvine) 4, 37–51, https://doi.org/10.4236/alc.2015.43006 (2015). · DOI
- Zhang, D. et al. PGRMC1 Is a Novel Potential Tumor Biomarker of Human Renal Cell Carcinoma Based on Quantitative Proteomic and Integrative Biological Assessments. PLoS One 12, e0170453, https://doi.org/10.1371/journal.pone.0170453 (2017). · DOI
- Sung, Y. H. et al. Knockout mice created by TALEN-mediated gene targeting. Nat Biotechnol 31, 23–24, https://doi.org/10.1038/nbt.2477 (2013). · DOI
- Doyle, E. L. et al. TAL Effector-Nucleotide Targeter (TALE-NT) 2.0: tools for TAL effector design and target prediction. Nucleic Acids Res 40, W117–122, https://doi.org/10.1093/nar/gks608 (2012). · DOI
Cited by
Sorted by citations
Lizama, B. N., Kahle, J., Catalano, S. M., Caggiano, A. O., Grundman, M., & Hamby, M. E. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076251 · Cited by 54
Metadata
- Authors
- Lee, S. R., Kwon, S. W., Kaya, P., Lee, Y. H., Lee, J. G., Kim, G., Lee, G.-S., Baek, I.-J., & Hong, E.-J.
- ORCID
- Lee, Geun-Shik
- Venue
- Scientific Reports
- Published
- 2018-10-24
- Volume
- 8
- Issue
- 1
- ISSN
- 2045-2322
- PMC
- PMC6200820
- Cited by
- 37
- References
- 4
- Language
- en
- Funders
- National Research Foundation of Korea (2014R1A1A2057405, 2015R1D1A1A01060335, 2018R1D1A1A02043102)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review