Zhidan Wu

TL;DR: SIRT1 is identified as a functional regulator of PGC‐1α that induces a metabolic gene transcription program of mitochondrial fatty acid oxidation in response to low glucose concentrations and has implications for understanding selective nutrient adaptation and how it might impact lifespan or metabolic diseases such as obesity and diabetes.

TL;DR: These results, together with previous findings, strongly suggest that TORCs play a key role in linking these external signals to the transcriptional program of adaptive mitochondrial biogenesis by activating PGC-1α gene transcription.

TL;DR: It is demonstrated that SIRT4 inhibition increases fat oxidative capacity in liver and mitochondrial function in muscle, which might provide therapeutic benefits for diseases associated with ectopic lipid storage such as type 2 diabetes.

TL;DR: It is suggested that therapeutic approaches that simultaneously stimulate mitochondrogenesis and reduce muscle proteolysis and inflammation have potential for treating sarcopenia.

TL;DR: It is demonstrated that pharmacological activation of PPARδ induces FAO via PGC-1α, however, PPAR δ agonism does not induce mitochondrial gene expression and function.