Heat Stress Declines Milk Protein Synthesis By Changing Metabolism Of Protein And Inducing Of Apoptosis Of Mammary Cell

The aim of this experiment it to research the relationship of decline of milk protein content and yield, digestibility, rumen formation, metabolism, hormone and pathway involved in synthesis of milk protein, and apoptosis of mammary cell of heat-stressed cows, and find the facters caused the decrease of milk protein content and yield. Four lactating Holstein cows(101±10 DIM, 574±36 kg of BW, 38±2.4 kg of milk/d) were randomly assigned to four environmental chambers and divided into two groups, for two experimental periods of 18 d(control period 9 d, trail period 9 d). A crossover design was used and period 1 and 2 were separated by 30 d. Cows in control period of both period 1and 2 were exposed to constant thermal neutral(TN) conditions[20°C, 55% humidity; temperature-humidity index(THI) = 65.5; 12 h light and dark cycles] and allowed to eat ad libitum for 9 d. Trial period of both period 1 and 2 included HS(n=2) group and pair-fed TN(PFTN, n=2) group and two groups exposed to HS [0600-1800 h 36°C, 1800-0600 h 32°C, 40% humidity; THI = 84.5; 12-h light and dark cycles] and TN respectively. The pattern and magnitude of reduced feed intake in the PFTN cows mirrored that of the HS cows. The results are as follows.1. Compared to PFTN, HS decreased milk protein yield(17.7%) and content(4.1%)(P<0.05). HS increased prior to feeding rumen liquid NH3-N concentration compared to PFTN. MCP(microbial crude protein), estimated by urinary excretion of purine derivatives, absorbed by intestine was not different between HS and PFTN cows. HS decreased plasma AA(total AA and 5 specific of free AA)(P<0.05) and plasma glucose(P<0.1), and tended to increase BUN and increased urea nitrogen in urine(UUN) and decreased NEFA.2. Heat stress decreased the milk protein yield and content(P<0.05), but had no influence on JAKSTAT pathway and expression of CSN3 which encodes for κ-casein. Heat stress increased the expression of m TOR(P<0.05), and had the tendency to increase the expression of S6K1(P<0.1). Heat stress increased the expression of CASP3 and COX2 involved in apoptosis(P<0.05).In conclusion,(1) The decrease of DMI can not account for the decline of milk protein yield and content thoroughly. Decrease of the content of milk protein precursor, plasma AA(P<0.05) and plasma glucose(P<0.1), and increase trend of BUN and the increase of UUN as well as decrease of NEFA indicated that milk protein precursor, plasma AA, may be the main source of energy substrates(not NEFA) in the heatstressed cow, which would normally be destined for milk protein synthesis, reducing the precursor pool for the synthesis of milk proteins and their yield.(2) Apoptosis of the mammary cells and decrease of the quantity could have synthesized milk protein caused by heat stress may account for the decline of milk protein yield and content, however, regulating the capacity of individual mammary cells by heat stress may not be the reason of decline of milk protein.