Hormonal
The PPARδ agonist GW501516 increases fatty acid oxidation in human skeletal muscle through a mechanism that requires both PPARδ expression and functional AMPK.
This study shows that maximizing fat oxidation in muscle cells requires both PPARδ and AMPK to be active. While GW501516 is not a consumer product, this suggests that natural methods activating both pathways (like high-intensity exercise which activates AMPK and can upregulate PPARδ over time) are synergistic for lipid metabolism.
Furthermore, we have shown that the subsequent increase in fatty acid oxidation induced by GW501516 is dependent on both PPARδ and AMPK.
Why this rating
In vitro human myocyte model with rigorous siRNA validation of mechanisms.
Source
Role of AMP Kinase and PPARδ in the Regulation of Lipid and Glucose Metabolism in Human Skeletal Muscle
David Kramer et al. · Journal of Biological Chemistry · 2007
DOI 10.1074/jbc.m702329200
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