Heonjoong Kang

TL;DR: It is shown here that targeted activation of PPARδ in adipose tissue specifically induces expression of genes required for fatty acid oxidation and energy dissipation, which in turn leads to improved lipid profiles and reduced adiposity.

TL;DR: The engineering of a mouse capable of continuous running of up to twice the distance of a wild-type littermate is described, achieved by targeted expression of an activated form of peroxisome proliferator-activated receptor δ (PPARδ) in skeletal muscle, which induces a switch to form increased numbers of type I muscle fibers.

TL;DR: It is found that PPARbeta/delta agonist and exercise training synergistically increase oxidative myofibers and running endurance in adult mice and demonstrates that AMPK-PPARdelta pathway can be targeted by orally active drugs to enhance training adaptation or even to increase endurance without exercise.

TL;DR: It is shown that PPARδ (NR1C2) knockout mice are metabolically less active and glucose-intolerant, whereas receptor activation in db/db mice improves insulin sensitivity, and gene array and functional analyses suggest that PParδ ameliorates hyperglycemia by increasing glucose flux through the pentose phosphate pathway and enhancing fatty acid synthesis.

TL;DR: It is demonstrated that in macrophages, VLDL functions as a transcriptional regulator via the activation of the nuclear receptor peroxisome proliferator-activated receptor δ, which reveals a pathway through which dietary triglycerides and V LDL can directly regulate gene expression in atherosclerotic lesions.