AI Insight
Researchers have identified SLC25A35 as the transporter responsible for exporting phosphoenolpyruvate (PEP) from mitochondria to the cytoplasm. This discovery reveals a previously unknown role for mitochondrial PEP synthesis in glyceroneogenesis, the metabolic pathway that produces glycerol-3-phosphate for fat storage in adipose tissue. The findings also implicate this pathway in the development of fatty liver disease, connecting mitochondrial metabolism to lipid homeostasis in a new way.
Why it matters
Understanding how mitochondrial PEP export contributes to fat metabolism and fatty liver disease could open new avenues for therapeutic intervention in metabolic conditions such as non-alcoholic fatty liver disease and obesity-related disorders.
Mitochondria generate phosphoenolpyruvate (PEP), although its export mechanism and physiological roles were unknown. In this issue of Cell, Kajimura and colleagues identify SLC25A35 as the mitochondrial PEP exporter and uncover a previously unrecognized role for mitochondrial PEP synthesis in glyceroneogenesis in adipose tissue and upon development of fatty liver disease.