Role of LXRs in control of lipogenesis.

By J. Schultz, H. Tu, Alvin Luk, J. Repa, J. Medina, Leping Li, S. Schwendner, Shelley Wang, M. Thoolen, D. Mangelsdorf and 2 more. Genes & Development, 2000

1,729 citations recorded by the source corpus.

The discovery of oxysterols as the endogenous liver X receptor (LXR) ligands and subsequent gene targeting studies in mice provided strong evidence that LXR plays a central role in cholesterol metabolism. The identification here of a synthetic, nonsteroidal LXR-selective agonist series represented by T0314407 and T0901317 revealed a novel physiological role of LXR. Oral administration of T0901317 to mice and hamsters showed that LXR activated the coordinate expression of major fatty acid biosynthetic genes (lipogenesis) and increased plasma triglyceride and phospholipid levels in both species. Complementary studies in cell culture and animals suggested that the increase in plasma lipids occurs via LXR-mediated induction of the sterol regulatory element-binding protein 1 (SREBP-1) lipogenic program.

Subfields: Molecular Biology, Oncology, Surgery

View Paper: https://www.semanticscholar.org/paper/e4cf93cbf7784b6aa2dc0a6db19e801eb0456056

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. P. Tontonoz
2. Christopher K. Glass
3. D. Mangelsdorf
4. A. Calkin
5. J. Goldstein
6. Michael S. Brown
7. P. Ferré
8. F. Foufelle

In Oncology

1. P. Tontonoz
2. J. Goldstein
3. D. Mangelsdorf
4. Michael S. Brown
5. A. Calkin
6. J. Repa
7. Christopher K. Glass
8. Johan Auwerx

In Surgery

1. P. Tontonoz
2. J. Goldstein
3. Michael S. Brown
4. D. Mangelsdorf
5. A. Calkin
6. F. Foufelle
7. P. Ferré
8. Christopher K. Glass

Citations in the corpus

• Mechanisms of Hepatic Triglyceride Accumulation in Nonalcoholic Fatty Liver Disease (2013, neutral): “As described above, insulin facilitates de novo lipogenesis through upregulation and activation of SREBP1c and induction of ACC.”
• Liver X receptor signaling pathways in cardiovascular disease. (2003, background): “cholesterol absorption in mice (13, 14) has triggered”
• Bile acids lower triglyceride levels via a pathway involving FXR, SHP, and SREBP-1c. (2004, background): “org Volume 113 Number 10 May 2004 1413 As expected, SREBP-1c promoter activity is induced by overexpression of the RXR/LXRα heterodimer in rat hepatoma McA-RH7777 cells in the presence of a natural LXR agonist and a synthetic RXR ligand (10, 11, 34).”
• The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, background): “SREBP-1 is a transcriptional factor present as three isoforms: while SREBP-1c regulates the activation of DNL and is stimulated by insulin [24], SREBP-2 is involved in cellular cholesterol homeostasis, therefore their dysregulation is involved in hepatic fat accumulation [17].”