Abstract #W79
Section: Physiology and Endocrinology (posters)
Session: Physiology and Endocrinology 2
Format: Poster
Day/Time: Wednesday 7:30 AM–9:30 AM
Location: Exhibit Hall A
Session: Physiology and Endocrinology 2
Format: Poster
Day/Time: Wednesday 7:30 AM–9:30 AM
Location: Exhibit Hall A
# W79
Post-ruminal choline supply during a feed restriction-induced negative nutrient balance alters components of hepatic mechanistic target of rapamycin (mTOR) signaling and plasma amino acids in Holstein cows.
D. N. Coleman*1, E. Abdelmaksoud2, R. Bucktrout1, Y. Liang1, M. Miura3, J. J. Loor1, 1University of Illinois, Urbana, IL, 2Beni-Suef University, Beni-Suef, Egypt, 3Ajinomoto Co. Inc, Tokyo, Japan.
Key Words: amino acid, protein synthesis
Post-ruminal choline supply during a feed restriction-induced negative nutrient balance alters components of hepatic mechanistic target of rapamycin (mTOR) signaling and plasma amino acids in Holstein cows.
D. N. Coleman*1, E. Abdelmaksoud2, R. Bucktrout1, Y. Liang1, M. Miura3, J. J. Loor1, 1University of Illinois, Urbana, IL, 2Beni-Suef University, Beni-Suef, Egypt, 3Ajinomoto Co. Inc, Tokyo, Japan.
The objective was to investigate the effects of post-ruminal choline (CHL) supply during a feed restriction-induced negative nutrient balance (NNB) on hepatic abundance and phosphorylation of mTOR (mechanistic target of rapamycin)-related signaling proteins and plasma AA concentrations. Ten primiparous rumen-cannulated Holstein cows (158 ± 24 DIM) were used in a replicated 5 × 5 Latin square design with 4 d of treatment and 10 d of recovery (14 d/period). Treatments were unrestricted intake with abomasal infusion of water, restricted intake (R; 60% of net energy for lactation requirements to induce NNB) with abomasal infusion of water (R0) or R plus abomasal infusion of 6.25, 12.5, or 25 g/d CHL ion. Liver tissue was collected on d 5 after infusions ended and blood on d 1–5. Statistical contrasts were A0 vs. R0 (CONT1), R vs. the average of CHL dose (CONT2) and tests of linear and quadratic effects of CHL dose. Although R tended to decrease the ratio of p-mTOR:total (t) mTOR (CONT1; P = 0.08), ratios of p-RPS6KB1:tRPS6KB1, p-EEF2:tEEF2, and p-EIF2:tEIF2 were greater (P < 0.05). Among those, supply of CHL led to decreases in p-EEF2:tEEF2 (CONT2; P = 0.04), p-EIF2:tEIF2 (P < 0.001) and tended to decrease p-EIF4BP1:tEIF4BP1 (P = 0.07). However, the effect was quadratic only for p-EEF2:tEEF2 (P = 0.02) and p-EIF2:tEIF2 (P < 0.001), reaching a nadir at 6.25 to 12.5 g/d CHL ion. The ratio of p-RPS6KB1:tRPS6KB1 was not affected by supply of CHL and was close to 2-fold higher at 25 g/d CHL vs. A0. Plasma Met concentration decreased with R (CONT1; P < 0.001) but increased linearly with CHL (P = 0.03). Restriction also increased plasma 3-methyl-histidine (CONT1; P < 0.001). Data suggest that dephosphorylation of EEF2 due to enhanced CHL supply along with greater p-RPS6KB1 potentially helped maintain or increase protein elongation during NNB. This idea is partly supported by the increased circulating Met. However, changes in initiation factors and initiation binding proteins indicated that CHL did not enhance initiation of protein synthesis.
Key Words: amino acid, protein synthesis
