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Defective hepatic autophagy is observed in obesity and diabetes, whereas autophagy is inhibited by insulin in hepatocytes. Insulin-induced anti-autophagy is mediated by non-canonical Gαi3 signaling  via  an unknown mechanism. Previously, we identified the anti-autophagic activity of Tnfaip8  via  activation of mammalian target of rapamycin (mTOR) in the nervous system. Here, we demonstrate that insulin temporally induces Tnfaip8, which mediates the anti-autophagic action of insulin through formation of a novel ternary complex including Tnfaip8, phosphatidylethanolamine (PE) and Gαi3. Specifically, an X-ray crystallographic study of Tnfaip8 from  Mus musculus  (mTnfaip8) at 2.03 Å together with LC-MS analyses reveals PE in the hydrophobic cavity. However, an mTnfaip8 mutant lacking PE does not interact with Gαi3, indicating that the PE component is critical for the anti-autophagic action of mTnfaip8  via  interaction with Gαi3. Therefore, the mTnfaip8-PE complex may act as an essential upstream effector  via  ternary complex formation most likely with active Gαi3 during insulin-induced anti-autophagy.

The Tnfaip8-PE complex is a novel upstream effector in the anti-autophagic action of insulin