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A translation repressor, 4E-BP1, regulates the triglyceride level in rat liver during protein deprivation. | LitMetric

A translation repressor, 4E-BP1, regulates the triglyceride level in rat liver during protein deprivation.

Am J Physiol Endocrinol Metab

Department of Bioregulation, Institute for Advanced Medical Sciences, Nippon Medical School, Kawasaki, Kanagawa, Japan.

Published: May 2020

AI Article Synopsis

  • Protein deprivation in diets has been linked to fatty liver disease, but the specific molecular processes are not well understood.
  • A study focused on the protein 4E-BP1 found that a low-protein diet increased its levels and triglyceride accumulation in rat livers within just one day.
  • The reduction of 4E-BP1 in rats on a low-protein diet decreased triglyceride levels and increased the protein responsible for fatty acid oxidation, highlighting 4E-BP1's crucial role in fatty liver development under protein deficiency.

Article Abstract

Protein deprivation has been shown to induce fatty liver in humans and animals, but the molecular mechanisms underlying such induction are largely unknown. Our previous studies have shown that a low-protein diet increases eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) protein and triglyceride (TG) levels in rat liver. 4E-BP1 is known to repress translation by binding to eIF4E. There is also evidence indicating that 4E-BP1 regulates lipid metabolism. Here, we examined the role of 4E-BP1 on TG accumulation in the livers of rats under protein deprivation. The low-protein diet rapidly increased the hepatic 4E-BP1 mRNA level within 1 day, followed by the induction of hepatic TG accumulation. The knockdown of hepatic 4E-BP1 attenuated the TG accumulation in rat liver induced by the low-protein diet. 4E-BP1 knockdown also increased the protein level of carnitine palmitoyltransferase 1A (CPT1A), a regulator of fatty acid oxidation, in the liver of rats fed a low-protein diet. These results indicate that a low-protein diet increases the amount of 4E-BP1, leading to TG accumulation in rat liver. We thus conclude that 4E-BP1 plays an important role in inducing hepatic steatosis under protein deprivation.

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Source
http://dx.doi.org/10.1152/ajpendo.00464.2019DOI Listing

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