The Role of PPAR<svg     style="vertical-align:-3.636pt;width:11.1125px;" id="M1" height="15.0125" version="1.1" viewBox="0 0 11.1125 15.0125" width="11.1125"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.022,-0,0,-.022,.062,10.412)"><path id="x1D738" d="M377 450h126l-264 -401q0 -75 -21 -153q-12 -44 -36 -71t-56 -27q-27 0 -42 18.5t-15 42.5q0 34 30 89q9 16 32 50q21 31 29 46q13 91 13 208q0 45 -11 94q-11 47 -34 47q-38 0 -61 -81h-23q40 150 121 150q46 0 65 -34.5t19 -99.5q0 -54 -7 -125z" /></g>

		
	
</svg> in the Transcriptional Control by Agonists and Antagonists

<table>Structural formulas of LPA, alkyl-LPA, cPA,and rosiglitazone. LPA is made up of a glycerol backbone with a hydroxyl group, a phosphate group, and a long-chain saturated or unsaturated fatty acid. Alkyl-LPA is an alkyl-ether analog of LPA. Alkyl-LPA shows a higher potency than LPA at the intracellular LPA receptor PPAR<i>γ</i>. cPA is a naturally occurring acyl analog of LPA. cPA is a weak agonist of plasma membrane LPA receptors, whereas cPA is an inhibitor of PPAR<i>γ</i>. Rosiglitazone is a thiazolidinedione (TZD) class of antidiabetics and is full agonist of PPAR<i>γ</i>.</table>

PPAR Research

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Figure 1: The Role of PPAR<svg     style="vertical-align:-3.636pt;width:11.1125px;" id="M1" height="15.0125" version="1.1" viewBox="0 0 11.1125 15.0125" width="11.1125"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.022,-0,0,-.022,.062,10.412)"><path id="x1D738" d="M377 450h126l-264 -401q0 -75 -21 -153q-12 -44 -36 -71t-56 -27q-27 0 -42 18.5t-15 42.5q0 34 30 89q9 16 32 50q21 31 29 46q13 91 13 208q0 45 -11 94q-11 47 -34 47q-38 0 -61 -81h-23q40 150 121 150q46 0 65 -34.5t19 -99.5q0 -54 -7 -125z" /></g>

		
	
</svg> in the Transcriptional Control by Agonists and Antagonists 

PPAR Research

The Role of PPAR in the Transcriptional Control by Agonists and Antagonists

Figure 1