TAILIEUCHUNG - báo cáo khoa học: " Increased hepatic oxidative metabolism distinguishes the action of Peroxisome proliferator-activated receptor d from Peroxisome proliferatoractivated receptor g in the ob/ob mouse"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Increased hepatic oxidative metabolism distinguishes the action of Peroxisome proliferator-activated receptor d from Peroxisome proliferatoractivated receptor g in the ob/ob mouse | Research Increased hepatic oxidative metabolism distinguishes the action of Peroxisome proliferator-activated receptor d from Peroxsome proliferator-activated receptor g in the ob ob mouse Lee D Roberts David G Hassall Deborah A Winegar John N Haselden Andrew W Nicholls and Julian L Griffin Addresses Department of Biochemistry University of Cambridge Tennis Court Road Cambridge CB2 1QW UK. GlaxoSmithKline Investigative Preclinical Toxicology Park Road Ware SG12 0DP UK. GlaxoSmithKline 5 Moore Drive Research Triangle Park NC 277709-3398 USA. Correspondence Julian L Griffin. Email jlg40@ Published 7 December 2009 Received 24 August 2009 Genome Medicine 2009 1 115 doi gm115 Revised Accepted 7 December 2009 The electronic version of this article is the complete one and can be found online at http content 1 12 115 2009 Roberts et al. licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background The peroxisome proliferator-activated receptors PPARs are ligand-activated transcription factors and members of the nuclear receptor superfamily. The PPAR family consists of three members PPARa PPARg and PPARd. PPARd controls the transcription of genes involved in multiple physiological pathways including cellular differentiation lipid metabolism and energy homeostasis. The receptor is expressed almost ubiquitously with high expression in liver and skeletal muscle. Although the physiological ligands of PPARd remain undefined a number of high affinity synthetic ligands have been developed for the receptor as a therapeutic target for type 2 diabetes mellitus dyslipidemia and the metabolic syndrome. Methods In this study the metabolic role of PPARd activation has been investigated .

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