Molecular mechanisms related to increased hepatic fat content in response to excessive physical exercise.

The main objective was to verify the responses of autophagy and lipogenesis genes and proteins in the liver of mice submitted to the excessive downhill running protocol with (EE/Rapa) and without (EE) rapamycin administration, a drug able to inhibit the mTORC1 pathway. The main results were higher levels of glucose, insulin, cortisol, ALT, and cholesterol, an increase of Foxo1A phosphorylation for the EE/Rapa group; hepatic fat accumulation for the EE and EE/Rapa groups; downregulation of autophagic genes for all exercise groups. In summary, excessive exercise led to increased liver fat content. Although rapamycin was effective in inhibiting mTOR, the autophagy pathway was not upregulated.