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Energy source conditions the milk response to TOR amino acids in dairy cows.

S. I. Arriola Apelo



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Energy source conditions the milk response to TOR amino acids in dairy cows.
V. L. Pszczolkowski1,2, H. Hu2, B. D. Brown5, S. J. Halderson2, J. Zhang4, A. S. Munsterman3, S. I. Arriola Apelo*2,1. 1Endocrinology and Reproductive Physiology Graduate Training Program, University of Wisconsin-Madison Madison, WI, 2Department of Animal and Dairy Sciences, University of Wisconsin-Madison Madison, WI, 3Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison Madison, WI, 4Department of Animal Science, China Agricultural University Beijing, China, 5Tuskegee University Tuskegee, AL.

TOR-AA are those amino acids that stimulate the mechanistic target of rapamycin complex 1 (mTORC1), including Leu and Met. Insulin is required for TOR-AA stimulation of mTORC1. The objective of this study was to determine if energy source affects milk production response to TOR-AA and nonTOR-AA. We hypothesized that glucogenic energy, through stimulation of insulin, potentiates the effects of TOR-AA on milk protein synthesis in dairy cows. Six second lactation, ruminally cannulated Holstein cows (93 � 9 DIM) with the right-side carotid artery transposed to subcutaneous level were used in a 6 � 6 Latin square design with 12-d periods. Cows were fed a basal diet restricted in ME and MP by 11 and 30%, respectively, and supplemented with a rumen inert fat (FAT, 563 g/d) or abomasally infused with an isocaloric amount of glucose (GLUC, 1 kg/day). Under each energy background, cows were abomasally infused with water (CTRL, 8 L/d), the TOR-AA (Met 30 g/d, Leu 80 g/d, TOR), or the nonTOR-AA (His 20g/d, Lys 60 g/d, NTOR). Infusions were administered for 8 h/d. Feed intake and refusals were measured on d 9 and 10; composite milk samples were collected on d 9 p.m. through d 11 a.m. (4 milkings); timed serial blood samples were taken on d 11. Data were analyzed by 2-way ANOVA; means were separated by pre-planned contrasts adjusted by Bonferroni. Dry matter intake was unaffected by treatment (P > 0.1). GLUC increased arterial insulin by 0.3 ug/L (P < 0.001). There was an interaction between AA and energy for milk protein, lactose and de novo fat yield (P < 0.5). GLUC increased milk protein yield by 70 g/day as compared with FAT under TOR-AA (P < 0.047) but had no significant effect under CTRL or NTOR (P > 0.1). Surprisingly, GLUC also improved lactose (240 g/d, P < 0.001) and de novo fat (61 g/d, P < 0.001) yields under TOR, and de novo fat under NTOR (45 g/d, P = 0.003). In conclusion, GLUC mediated the milk component synthesis response to TOR-AA, suggesting an mTORC1 mediated effect of glucose or more specifically insulin and TOR-AA on milk production.

Keywords: amino acids, energy, mechanistic target of rapamycin complex 1 (mTORC1).