Fræðaþing landbúnaðarins - 04.02.2005, Síða 97

These tremendous changes call for a coordination of the biological processes in different
tissues resulting in metabolic changes (see table 1) that try to ensure that the cow’s
genetic potential for milk yield is exploited but at the same time maintaining
physiological homeostasis. When the regulatory mechanism fails one gets physiological
imbalance leading to high risk of disease.
Metabolic regulation and clinical biochemistry
The endocrine system plays an important role in the metabolic regulation. The hormonal
regulation comprises both homeorhesis and homeostasis. Bauman and Currie (1980)
defíned homeorhesis as ”the orchestrated or coordinated changes in the metabolism
necessary to support a physiological state”, with an adaptation to a new equilibrium
taking place over days or weeks. Homeorhesis is e.g. responsible for the different phases
in the production life of the cow. Homeostasis on the other hand can be defined as the
regulation that maintains the equilibrium of the animal in different nutritional and
environmental conditions; a regulation that takes place from minute to minute.
The ratio of growth hormone to insulin is high in blood of cows in early lactation, which
induces mobilisation of fatty acids ffom adipose tissue triglycerides (TG). The sensitivity
of the adipose tissue to lipolytic signals (epinephrine and norepinephrine) is also greatly
enhanced in early lactation (Theilgaard et al., 2002; Underwood et al., 2003). Fatty acids
released ffom adipose tissue circulate as nonesterified fatty acids (NEFA), which are a
major source of energy to the cow during this period. The percentage of blood NEFA
utilized by the liver is fairly constant, hence the concentration of NEFA in blood reflects
the degree of adipose tissue mobilisation (Pullen et al., 1989). In liver NEFA may be
transformed into triglycerides, be incorporated into lipoproteins and released into the
circulation, be oxidized for energy or be converted to ketone bodies.
Consequently, stressors and poor nutritional management causing reduction in voluntary
dry matter intake (DMI) will result in large increases in NEFA around calving (Drackley,
1999; Ingvartsen and Andersen, 2000). The levels then decrease gradually in the first six
weeks of lactation with cows developing ketosis decreasing more slowly (Schwalm and
Schultz 1976).
The use of glucose is reduced in most tissues in early lactation and instead the use of fatty
acids and ketone bodies is increased. Despite the reduced use of glucose and a
considerable increase in the gluconeogenesis in liver and kidney, the glucose
concentration normally drops in early lactation.
The principle precursors of ketone bodies are butyrate ffom the rumen and NEFA derived
ffom fat mobilisation. The major tissues involved are the liver and the rumenoreticulum
epithelium. Butyrate is metabolised into beta-hydroxy-butyrate (BHB) on absorption
ffom the rumen. This BHB production forms the basal concentration of ketone bodies in
ruminants. The ketogenesis in hepatic tissue generally increases the level of ketone
bodies in blood. The concentration of ketone bodies in blood is determined by production
rate rather than utilization as they go hand in hand until a point is reached when
utilisation is maximised (Bergman 1971).
Several workers have found that in normal cows the ketone bodies in blood rise gradually
ffom calving, reaching a peak 20-30 days postpartum and drop after that. This being a
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