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Web Desc
PPAR/LXR
joint with Bioactive Lipids, Lipidomics and their Targets
Organizer(s): Christopher Glass and Mitchell A. Lazar
Date: April 12 - 17, 2005
Location: Fairmont Chateau Whistler, Whistler, BC, Canada
Part of the Translational Medicine Series, Supported by Pfizer Global Research and Development
Summary of Meeting:
The accelerating incidence of obesity, insulin resistance and hyperlipidemia in Westernized societies and the attendant complications of diabetes and atherosclerosis is fueling an explosion of interest in the molecular mechanisms underlying metabolic disease. The PPAR subfamily of nuclear receptors, consisting of PPARa, PPARg, and PPARd, initially became the focus of intense investigation following discoveries of roles of PPARa and PPARg in controlling aspects of lipid and glucose homeostasis. PPARs regulate programs of gene expression by functioning as ligand-dependent transcription factors. Although the range of physiological ligands that regulate the activities of each PPAR in vivo remain to be clearly defined, PPARa and PPARg are the molecular targets of fibrates and thiazolidinediones that were identified empirically to lower circulating triglyceride levels and to improve insulin resistance in diabetic patients, respectively. The recognition that these classes of drugs exert their therapeutic effects by binding to PPARa and PPARg suggests that more effective drugs for the treatment of hyperlipidemia and type 2 diabetes can be developed by optimizing ligand-receptor interactions. Furthermore, recent studies have suggested additional roles of PPARs in a diverse range of physiological and pathophysiological settings, including vascular wall biology, placental physiology, atherosclerosis, inflammatory bowel and skin disorders, metabolic bone disease and cancer. Further exploration of these observations should expand our general understanding of important developmental and homeostatic processes at a molecular level, and may lead to new avenues of therapeutic intervention in common human diseases. Because of the potential biomedical significance of this field of research, studies of PPAR-related processes have resulted in a number of pioneering discoveries of general importance to molecular biology and development. In concert with recent developments in the PPAR field, a parallel of series of discoveries has emerged relating to regulation of cholesterol and triglyceride homeostasis by the LXR subfamily of nuclear receptors, consisting of LXRa and LXRb. The LXRs are activated by cholesterol metabolites and provide the basis for a feed-forward homeostatic control circuit for maintenance of cellular cholesterol levels. The biological actions of LXRs relate in part to their ability to regulate members of the ABC family of lipid transporters, including ABC A1 and ABC G1, which mediate the efflux of cholesterol from cells. These findings raise the possibility that new classes of cholesterol lowering drugs could be developed that would work synergistically with currently available agents. These considerations justify a Keystone Conference focused on PPARs and LXRs in 2005. The PPAR field is entering a new wave of discovery based on the recent success in generating conditional experimental systems for analysis of PPARg and PPARd-null mice. Studies for metabolic pathways regulated for PPARs and LXRs are also benefiting from the application of increasingly powerful genomics and proteomics tools. A 2005 Keystone Meeting on PPARs and LXRs will be well timed to bring together a diverse array of investigators from academia and industry to synthesize the most recent developments and define future directions. This meeting will also provide opportunities to highlight major findings from studies of less well-characterized members of the nuclear receptor family that have recently emerged as potential regulators of lipid metabolism and energy homeostasis, such as FXR. Finally, this meeting will continue to be a valuable opportunity for trainees to present work in a poster session, meet leaders in the field, and explore opportunities for future career development.
Discounted Abstract Deadline: December 13 2004
Discounted Registration Deadline: February 14 2005
We gratefully acknowledge additional support for this conference from:
Pfizer Global Research & Development
We gratefully acknowledge additional in-kind support for this conference from those foregoing speaker expense reimbursements:

Exelixis, Inc.

GlaxoSmithKline

Merck Research Laboratories
We gratefully acknowledge the generous grant for this conference provided by:

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Grant No. 1R13-DK070428-01
We appreciate the organizations that provide Keystone Symposia with additional support, such as marketing and advertising:

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Special thanks to the following for their support of Keystone Symposia initiatives to increase participation at this meeting by scientists from underrepresented backgrounds:

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