Fig. 7.

Schematic representation of the proposed role of ANGPTL4 in providing lipid to exercising muscle. During exercise, circulating FFAs and VLDL particles are directed to exercising and nonexercising muscle. In the nonexercising leg, increased FFA levels provoke an increase in ANGPTL4 expression via PPARδ, leading to inhibition of LPL activity and consequent reduction in uptake of fatty acids derived from VLDL, which likely is aimed at preventing lipid overload. In contrast, in the exercising leg the stimulatory effect of FFA on ANGPTL4 mRNA is counteracted by AMPK-mediated suppression of ANGPTL4 mRNA. As a result, LPL activity remains high, allowing full exploitation of fatty acids derived from VLDL as the substrate for fatty acid oxidation to meet the energetic needs of exercising muscle.