Stereology shows that damaged liver recovers after protein refeeding

Gomes, Silvio Pires; Silva, Andréa Almeida Pinto da; Crisma, Amanda Rabello; Borelli, Primavera; Hernandez‐Blazquez, Francisco Javier; Melo, Mariana Pereira de; Bacci, Barbara; Loesch, Andrzej; Ribeiro, Antônio Augusto Coppi Maciel

doi:10.1016/j.nut.2017.02.010

Cited by 4 publications

(1 citation statement)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Among those, an increase in the demand of aa, as building blocks of proteins, has been described 18 . A recent study showed that protein restriction in mice decreases the volume of both the liver and hepatocytes, and these defects were not completely reversed by aa restoration in the diet 19 . Hence, we can speculate that a deficiency in dietary protein intake could exert a strong and lasting impact on the capacity of recovery in cases of hepatocellular deterioration.…”

Section: Discussionmentioning

confidence: 99%

Amino acid-induced regulation of hepatocyte growth: possible role of Drosha

et al. 2019

View full text Add to dashboard Cite

In an adult healthy liver, hepatocytes are in a quiescent stage unless a physical injury, such as ablation, or a toxic attack occur. Indeed, to maintain their crucial organismal homeostatic role, the damaged or remaining hepatocytes will start proliferating to restore their functional mass. One of the limiting conditions for cell proliferation is amino-acid availability, necessary both for the synthesis of proteins important for cell growth and division, and for the activation of the mTOR pathway, known for its considerable role in the regulation of cell proliferation. The overarching aim of our present work was to investigate the role of amino acids in the regulation of the switch between quiescence and growth of adult hepatocytes. To do so we used non-confluent primary adult rat hepatocytes as a model of partially ablated liver. We discovered that the absence of amino acids induces in primary rat hepatocytes the entrance in a quiescence state together with an increase in Drosha protein, which does not involve the mTOR pathway. Conversely, Drosha knockdown allows the hepatocytes, quiescent after amino-acid deprivation, to proliferate again. Further, hepatocyte proliferation appears to be independent of miRNAs, the canonical downstream partners of Drosha. Taken together, our observations reveal an intriguing non-canonical action of Drosha in the control of growth regulation of adult hepatocytes responding to a nutritional strain, and they may help to design novel preventive and/or therapeutic approaches for hepatic failure.

show abstract

Section: Discussionmentioning

confidence: 99%