Dynamic model of the lactating dairy cow metabolism

Abstract

The whole-animal model described in this paper is intended to be a research model with an intermediary structure between sophisticated and simple cow models. The mechanistic model structure integrates the main metabolic pathways of the lactating dairy cow. Milk yield and related feed intake for varying production potentials were considered to be the driving forces and were empirically defined. The model was designed to explain the main metabolic flows and variations in body reserves associated with the push of nutrients from dry matter intake and their pull by the mammary gland to synthesise milk components throughout lactation. The digestive part of the model uses either known feed unit systems (e.g. PDI system for protein) or published empirical equations for the prediction of digestive flows of organic matter, starch and fatty acids and ruminal volatile fatty acid production. The metabolic sub-system is made up of four tissue compartments (body protein, body lipid, protein in the uterus and triglycerides in the liver) and five circulating metabolites (glucose, amino acids, acetate 1 butyrate, propionate, and triglycerides and non-esterified fatty acids). A major original aspect of the model is its homeorhetic control system. It was assumed that flows relating to adipose and protein tissue anabolism and catabolism were driven by a couple of linked theoretical hormones controlling mobilisation and anabolism. The evolution in body composition and body weight were outcomes of this control. Another originality of the model is its suitability for milk yields varying from 10 to 50 kg at peak production. This was achieved by homeorhetic control of milk potential acting on several key metabolic flows. Homeostatic regulation was also introduced in order to confine the behaviour of the model within realistic physiological values. For some basic aspects (e.g. Uterine involution, standard kinetics of body protein and fat), it was necessary to build specific databases from the literature and interpret these by meta-analysis. Fairly realistic simulated kinetics were obtained for body composition, liver triglycerides, blood plasma metabolite concentrations, milk protein and fat contents, and also for major groups of milk fatty acids.

Advances in predicting nutrient partitioning in the dairy cow: recognizing the central role of genotype and its expression through time

“…In the majority of mechanistic metabolic models (Danfaer, 1990;Baldwin, 1995;Martin and Sauvant, 2007), lactational profiles of potential milk fat, protein and lactose are directly linked to the milk production potential or mammary cell number trajectory and rely on nutrient supply-driven partition to generate differences in milk composition. This has been shown to be less than satisfactory and led to modifications in the representation of the potential milk composition profiles with, for example, a dissociation of milk lactose production from milk fat and protein production (Hanigan et al, 2007).…”

“…In the same way, there have been no explicit homeorhetic trajectories for body reserve usage in the majority of metabolic models, with one exception (Martin and Sauvant, 2007). Taking Molly as an example, changes in body lipid reserves are driven by the size of the glucose pool relative to a reference value, with excess glucose favouring lipid accretion and glucose shortage provoking lipolysis (Baldwin, 1995).…”

A teleonomic model describing performance (body, milk and intake) during growth and over repeated reproductive cycles throughout the lifespan of dairy cattle. 1. Trajectories of life function priorities and genetic scaling

“…Through this mechanistic representation, variations of wholeanimal performance emerged from the aggregation of several points of biochemical regulation. Similar attempts to incorporate regulation rules in animal models through control variables driving physiological processes were performed in several other studies, for example, 'lactation hormone' (Neal and Thornley, 1983;Baldwin et al, 1987c), 'anabolic and catabolic hormones' (Sauvant and Phocas, 1992;Baldwin, 1995;Martin and Sauvant, 2007) and 'growth hormone and insulin' (Danfaer, 1990).…”

“…Further developments were carried out by Dijkstra et al (1997), Vetharaniam et al (2003a and2003b) and Pollott (2004). This principle of modelling was also used to direct adipose tissue anabolism and catabolism (Sauvant and Phocas, 1992;Baldwin, 1995;Martin and Sauvant, 2007) or to provide kinetics of plasma growth hormone and insulin driving exchanges between the tissues and udder (Danfaer, 1990). However, none of these approaches focused on a centralized regulating model.…”

“…The model can be used as a 'virtual cow' to simulate individual lifetime performance, formalize hypotheses and provide inputs to run scientific models focusing on particular physiological aspects, such as the control of fertility or the description of main metabolic pathways associated with performance (Martin and Sauvant, 2007). For instance, a model of reproduction predicting conception times could use simulations of milk yield, intake and body reserves as predictors and in turn set the timing of reproductive events.…”