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Energy intake modulates intramuscular mTORC1 signaling and ubiquitin‐mediated proteolysis during energy deficit independent of dietary protein variations
Author(s) -
Carbone John Walter,
Margolis Lee M,
McClung James P,
Cao Jay J,
Young Andrew J,
Pasiakos Stefan M
Publication year - 2013
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.27.1_supplement.631.1
Subject(s) - mtorc1 , p70 s6 kinase 1 , endocrinology , medicine , phosphorylation , protein kinase b , proteolysis , skeletal muscle , downregulation and upregulation , protein degradation , chemistry , biology , biochemistry , enzyme , gene
Effects of variations in habitual and acute dietary protein consumption on intracellular regulators of human skeletal muscle mass during energy deficit (ED) were investigated. Using a randomized‐block design, 32 men and 7 women consumed diets providing protein at 0.8, 1.6, or 2.4 g·kg −1 ·d −1 for 31 days. A 10‐day weight maintenance (WM) period preceded 21 days of ED, during which energy intake was reduced to 60% of daily requirements. Phosphorylation of mTORC1 associated signaling proteins, protein ubiquitylation (Ub), and NFκB expression were assessed in vastus lateralis muscle samples obtained after an overnight fast (FAST) and again 120 min after consuming a mixed meal (480 kcal, 20 g protein; FED) on days 10 and 31. Independent of dietary protein level and feeding state, Ub was 25% higher ( P < 0.05) for ED versus WM. Energy state and feeding altered p70 S6K1 phosphorylation, as FED‐ED levels were 26% lower than FED‐WM (energy‐by‐feeding, P < 0.05). Overall, Akt and rpS6 phosphorylation were higher ( P < 0.05), and NFκB and Ub were lower ( P < 0.05), for FED versus FAST. These data suggest that ED may upregulate intramuscular ubiquitin‐mediated proteolysis, and attenuate p70 S6K1 sensitivity to feeding, although energy consumption, independent of habitual protein intake, may confer skeletal muscle protection through concomitant stimulation of mTORC1 signaling and inhibition of Ub during ED. Supported by USAMRMC, EMU CHHS SSSA, and USDA ARS