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. 2013 Apr 29;2013:684159. doi: 10.1155/2013/684159

Table 1.

Activation of PPAR isotypes in ruminants by main long-chain fatty acids or glucose.

LCFA/glucose Effect on PPAR isotype@ Method# References
PPARα PPARγ PPARβ/δ
16:0 +++ +++ n/a Indirect [26, 28, 61]
18:0 +++ +++ n/a Indirect [26, 28]
c9-18:1 ++ + n/a Indirect/Luciferase [26, 28, 62]
t10-18:1 n/a& + n/a Indirect [26]
18:2 + n/a n/a Indirect [26, 28]
c9,t11-18:2 + n/a n/a Indirect [26, 28]
t10,c12-18:2 + ± n/a Indirect [26, 28]
CLAmix$ + n/a n/a Indirect [36, 77]
20:0 ++ n/a n/a Indirect [26, 28]
20:4n-6 ++ n/a ++* Indirect/Luciferase [68, 77]
20:5n-3 ++ ++ n/a Indirect [26, 28]
22:6n-3 + n/a n/a Indirect [26, 28]
Glucose No n/a ++ Luciferase [68]

@+++: strong agonist; ++: agonist; +: weak agonist; ±: mixture between agonist and antagonist.

*The 12-HETE, a metabolite of the 20:4n-6 is the actual agonist.

#Indirect: the effect on PPAR isotype target genes was uncovered by the use of specific PPAR synthetic agonists; luciferase: the use of the PPRE-luciferase construct to test activation of PPAR by agonists.

$A mixture (ca. 50% each) of the t10,c12- and c9,t11-conjugated 18:2

&Not available.