Premium
A high protein diet strongly inhibits hepatic proteolysis in rats
Author(s) -
Chotechuang Nattida,
Bos Cécile,
AzzoutMarniche Dalila,
Chevalier Laure,
Luengo Catherine,
Tomé Daniel,
Gaudichon Claire
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a333
Subject(s) - proteolysis , medicine , phosphorylation , endocrinology , protein turnover , protein degradation , western blot , biology , kidney , skeletal muscle , ampk , calpain , enzyme , chemistry , biochemistry , protein kinase a , protein biosynthesis , gene
The metabolic effects of high protein (HP) diets on individual tissues have been poorly studied. We previously showed that a HP diet led to a tissue‐specific decrease in liver and kidney protein synthesis rates associated with a significantly increased hepatic protein pool. Here, we measured protein degradation in liver, kidney and skeletal muscle ex‐vivo from fasted or fed rats adapted to normal or high protein diets for 14 d (NP and HP, 13% or 49% of energy, n=50). The tissue expression of genes involved in the main proteolytic pathways was assessed by real‐time PCR. Western‐blot analysis allowed to study the activation of effectors involved in amino acid signalling pathways. Liver protein degradation rate was significantly decreased by 16% and 47% in the fasted and fed state, respectively in HP rats compared to NP rats. Kidney and muscle degradation rates were not influenced by the diet. Gene expressions of ubiquitin, E2 enzyme, proteasome subunits, cathepsine B, m‐calpain were not influenced by the diet. Conversely the HP diet was associated with a significant decrease of AMPk phosphorylation, a higher phosphorylation of both mTOR and 4EBP1 and a decrease of GCN2 and eIF2 phosphorylation in the liver. These results suggest that the main metabolic effects of HP diets are a strong inhibition of liver proteolysis, consistent with the mTOR activation and the increased hepatic protein accretion previously observed.