A. Withy

Capacity-Contribution Paradox: Fatty Acid Oxidation Compensates for Low Glucose-Derived Acetyl-CoA in Cancer.

This study reveals that fatty acid oxidation (FAO) in cancer cells primarily compensates for low glucose-derived acetyl-CoA by supporting mitochondrial metabolism through a malic enzyme-dependent shunt, rather than serving as a primary fuel source.

CPT1a regulates the delivery of extracellular fatty acids for cardiolipin turnover in prostate cancer cells.

The paper shows that CPT1a regulates the uptake of extracellular fatty acids into mitochondria for cardiolipin remodeling in prostate cancer cells, despite these fatty acids being minor contributors to the TCA cycle.