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. 2020 Feb 4;3(3):e202000646. doi: 10.26508/lsa.202000660

Figure 7. Working model proposal of the beneficial effects of high-diet in the dystrophic milieu.

Figure 7.

A short-term high-fat diet (HFD) regimen provides a beneficial metabolic reprogramming of skeletal muscle interstitial fibro/adipogenic progenitors, dramatically affected in Duchenne muscular dystrophy. HFD restores the proper metabolic signature of dystrophic fibro/adipogenic progenitors, fueling mitochondrial pathways of fatty acid oxidation and tricarboxylic acid cycle and modulating the glycolytic flux. From the molecular point of view, β-catenin is a crucial hub that modulates muscle stem cells behavior. β-catenin inhibitors casein kinase (CK1) and MEST are repressed by HFD. The inhibition of glycogen synthase kinase 3 beta (GSK-3β) activates the β-catenin signaling in turn modulating follistatin (Fst) expression Fst, in concert with IGF1, is released to sustain the differentiation of muscle satellite cells and myotube hypertrophy. The beneficial effects of HFD lead to the amelioration of the dystrophic phenotype.