The elusive endogenous adipogenic PPARγ agonists: Lining up the suspects

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• 作者：Philip Hallenborg^a ; ^b ; Rasmus K. Petersen^a ; Irene Kouskoumvekaki^c ; John W. Newman^d ; ^e ; Lise Madsen^a ; ^f ; Karsten Kristiansen^a ; ^{kk@bio.ku.dk" class="auth_mail" title="E-mail the corresponding author}
• 关键词：NO ; nitric oxide ; NO2 ; dioxide radical ; O2 ; superoxide ; ONO2&minus ;   ; peroxynitrite ; 15-dPGJ2 ; 15-deoxy-Δ12 ; 14-prostaglandin J2 ; AA ; arachidonic acid ; ADH ; alcohol dehydrogenase ; AF-1 ; ligand-independent activation function ; AF-2 ; ligand-dependent activation function ; azPC ; azelayol phosphatidylcholine ; BAT ; Brown adipose tissue ; CBR ; carbonyl reductase ; C/EBP ; CCAAT/enhancer binding protein ; ChREBP ; carbohydrate element binding protein ; COX ; cyclooxygenase ; CPA ; cyclic phosphatidic acid ; c
• 刊名：Progress in Lipid Research
• 出版年：2016
• 出版时间：January 2016
• 年：2016
• 卷：61
• 期：Complete
• 页码：149-162
• 全文大小：1229 K

文摘

The nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ) is the key decisive factor controlling the development of adipocytes. Ligand-mediated activation of PPARγ occurs early during adipogenesis and is thought to prime adipose conversion. Although several fatty acids and their derivatives are known to bind to and activate PPARγ, the identity of the ligand(s) responsible for initiating adipocyte differentiation is still a matter of debate. Here we review recent data on pathways involved in ligand production as well as possible endogenous, adipogenic PPARγ agonists.