A nuclear-receptor-dependent phosphatidylcholine pathway with antidiabetic effects
Jae Man Lee,
Yoon Kwang Lee,
Jennifer L. Mamrosh,
Scott A. Busby,
Patrick R. Griffin,
Manish C. Pathak,
Eric A. Ortlund and
David D. Moore ()
Additional contact information
Jae Man Lee: Program in Developmental Biology, Baylor College of Medicine
Yoon Kwang Lee: Baylor College of Medicine
Jennifer L. Mamrosh: Baylor College of Medicine
Scott A. Busby: The Scripps Research Molecular Screening Center, The Scripps Research Institute, Scripps Florida, Jupiter, Florida 33458, USA
Patrick R. Griffin: The Scripps Research Molecular Screening Center, The Scripps Research Institute, Scripps Florida, Jupiter, Florida 33458, USA
Manish C. Pathak: Emory University School of Medicine
Eric A. Ortlund: Emory University School of Medicine
David D. Moore: Program in Developmental Biology, Baylor College of Medicine
Nature, 2011, vol. 474, issue 7352, 506-510
Abstract:
An antidiabetic LRH-1 agonist Excess liver fat, or steatosis, is an important risk factor for obesity-associated diabetes. A natural product, dilauroyl phosphatidylcholine (DLPC), has now been identified as a possible antisteatosis agent, with therapeutic potential in pre-diabetic people. DLPC activates the orphan nuclear receptor LRH-1, loss of which decreases bile acid levels. Elevated bile acid is known to decrease steatosis. Acting as an LHR-1 agonist, DLPC decreases hepatic steatosis and improves glucose homeostasis in mouse models of insulin resistance.
Date: 2011
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DOI: 10.1038/nature10111
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