FIGURE 6.

PGC-1α coordinates anabolic and catabolic pathways in skeletal muscle. The model integrates the findings of this study and shows the PGC-1α-mediated coordination of de novo lipogenesis, lipid accumulation, and lipid oxidation. Enzymes being activated by PGC-1α and regulating metabolic key steps are indicated in gray ovals (G6PDH, FAS, and carnitine palmitoyltransferase 1b (CPT-1b)). PGC-1α coordinates anabolic processes (lipogenesis and IMCL accumulation) and catabolic processes (β-oxidation, the Krebs cycle, and oxidative phosphorylation (OXPHOS)) in skeletal muscle. PGC-1α enhances glucose (Glu) uptake and flux through the pentose phosphate pathway. Concomitantly, NADP⁺ is reduced to NADPH, which serves as reducing agent for lipogenesis. De novo synthesized fatty acids (FA) are then stored as IMCL and serve as energy substrate during endurance exercise. By metabolizing lipids through β-oxidation, the Krebs cycle, and oxidative phosphorylation, ATP for muscle contraction is produced. The flux of glucose toward the pentose phosphate pathway also generates ribose 5-phosphate, which constitutes a structural element of ATP and other nucleotides.