The role of insulin in the regulation of milk protein synthesis in pasture-fed lactating ruminants : a thesis presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Animal Science at Massey University, Palmerston North, New Zealand
The primary aim of this thesis was to determine the role of insulin in milk protein production in pasture-fed lactating ruminants (ewes and cows), using the hyperinsulinaemic euglycaemic clamp (HEC) technique. Three experiments were carried out. In the first 2 experiments, the response of pasture-fed ewes and dairy cows to the HEC were established and compared to concentrate-fed ruminants (dairy cows and goats). Use of the HEC technique in pasture-fed ruminants did not result in an increase in milk protein yield or concentration. However, a reduction in feed intake along with maintenance of milk protein yield resulted in a change in efficiency of utilisation of dietary crude protein for milk protein production. This indicated that changes in blood insulin could result in changes in nutrient partitioning to maintain milk protein production. In Experiment 3, mechanisms were examined that could maintain milk protein production despite a reduction in feed intake. The arterio-venous concentration difference technique and a leucine tracer infusion were used to measure amino acid (AA) uptake and subsequent metabolism for milk protein production under conditions imposed by the HEC. This experiment demonstrated that the HEC reduced AA supply to the mammary gland and there was a decrease in the uptake of some AA. There was no increase in mammary blood flow to compensate for this. The deficit in the ratio of AA uptake to their secretion in milk protein suggests the use of plasma free AA concentrations underestimates uptake of AA by the mammary gland and there are contributions by alternative sources such as peptide AA and erythrocytes. There was no decrease in leucine oxidation in the mammary gland, indicating that AA were not conserved for milk protein production through an alteration in this mechanism. These results support the theory that the mammary gland has the ability to respond to modified precursor supply to maintain milk protein output.