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METABOLIC disease is most commonly seen around the periparturient period of a cow, due to the marked nutritional, metabolic, hormonal and immunological changes (Goff and Horst, 1997).

Metabolic diseases not only lead to direct costs, such as treatments and veterinary bills, but have knock-on, indirect costs on infertility and displaced abomasums, to name but a few. Not only do the cows have to cope with their metabolic insufficiencies, but, during the periparturient period, dairy cows experience a natural state of immunosuppression, increasing susceptibility to infections (Kehrli et al, 1989a).

Neutrophils undergo a weakening of their capacity to phagocytose (Kehrli et al, 1989), meaning the fight against bacteria is less effective. Inappetent cows produce non-esterified fatty acids (NEFAs), which impair lymphocyte proliferation and polymorpho-nuclear neutrophilic leukocyte function (Ster et al, 2012).

NEFAs bind to magnesium when mobilised in the bloodstream and so promote a state of hypomagnes-aemia, which, in turn, can lead to hypocalcaemia. If a cow is unable to maintain blood concentrations of calcium, magnesium, phosphorus and glucose using homeostatic mechanisms then metabolic disease develops, often setting off a cascade of disease.

Below the more common metabolic diseases are adressed – namely ketosis and fatty liver. These diseases combine and should not be diagnosed and treated as single entities, as the causes are often multi-factorial.

It is vital to carry out a full physical examination before any treatments, as cows may have concurrent pathology/ disease, such as fractures or ruptured tendons from falling/slipping, and these will need to be euthanised for welfare reasons immediately.

Energy requirements

In ruminants, glucose metabolism is unique as they absorb no preformed glucose from the gut. The main source of glucose is gluconeogenesis of volatile fatty acids (VFAs), primarily propionate, which are produced by bacterial fermentation in the rumen. The VFAs are absorbed and, via the bloodstream, end up in the liver where gluconeogenesis takes place.

It is commonly written all dairy cows suffer from ketosis at some point in their early lactation for a variety of reasons, with resulting economic losses to the farmer from treatment costs, decreased milk production, impaired reproduction efficiency and increased involuntary culling (Reist et al, 2000).

A 650kg cow walking to the field daily and producing 40 litres of milk a day will need around 285MJ/ day. If the energy content of the foodstuff is 10MJ/kg/dry matter (DM), such as grass, the cow will need to ingest 28.5kg DM, which is 4.4 per cent of the cow’s bodyweight – far exceeding the expected dry matter intake (DMI) of three per cent bodyweight.

The resulting negative energy balance will lead to type one ketosis, which is commonly seen from six weeks to eight weeks postparturition when feed intake (energy intake) is outstripped by milk output (energy output).


Type one ketosis occurs when there is not enough propionate to meet the glucose needs of the cow, as it is the major precursor for gluconeogenesis. There is little conversion of NEFAs to triglycerides, resulting in minimal fat infiltration of the liver, meaning the liver’s function is unimpaired. Ensuring a diet is sufficient in propionate avoids the use of other glucose precursors and subsequent mobilisation of peripheral adipose tissue. This can be achieve by adding FF CaPro to the diet.

Type two ketosis occurs when there is a primary problem such as fatty liver, metritis or hypocalcaemia and the cow is, therefore, unable or unwilling to eat sufficiently for its needs.

Fatty liver

Fatty liver disease is initiated by the ratio of growth hormone: insulin being high at calving, which, in turn, stimulates the mobilisation of NEFAs from adipose tissue to support the lactation energy requirements. Adipose lipogenesis ceases and there is an increased sensitivity to lipolytic signals, such as epinephrine.

Resistance to insulin develops, meaning all energy can be used for milk production. Consequently, stressors and poor nutritional management cause a decrease in voluntary DMI and a large increase in NEFAs immediately post-calving (Bertoni et al, 1998). The NEFAs are primarily absorbed by the liver, where they undergo three separate processes, as shown by figure 1.

  • Assuming there is sufficient propionate in the diet, by addition of FF CaPro, the free fats are oxidised into acetyl coenzyme A (CoA) and enter the Krebs cycle, which leads to the production of glucose.
  • If there is insufficient propionate, the acetyl CoA is metabolised to ketone bodies (acetoacetate and beta-hydroxybutyrate; BHB) which are then used as energy sources. Excess levels of these in the blood demonstrate more are being produced than are being used by the peripheral tissues. Ketones produced in the Iiver are limited to utilisation by heart, skeletal muscle, kidney, lactating mammary glands and intestinal tissues (Herdt, 1988). These tissues have the enzymes necessary to convert ketones back to acetoacetate and then to acetoacetyl CoA (Littledike et al, 1981).
  • If the uptake of NEFAs is greater than the number being oxidised then the NEFAs are re-esterified and ideally exported from the liver via low density lipoproteins. Ruminants are not very good at this, so the fats are slowly exported into the bloodstream and instead accumulate in the liver, reducing its capacity for gluconeogenesis. As a consequence, more peripheral fats are mobilised. The process is a vicious circle and results in a fatty liver with rounded edges that show how swollen the liver is and an abnormal colour.

Signs and diagnosis

The clinical signs for ketosis are often non-specific, such as anorexia with accompanying weight loss, decreased milk production and scant faeces. The smell of acetone (“pear drops”) is often reported, but is not a specific diagnosis. Some cows demonstrate nervous signs such as pica, ataxia and head pressing, which can last for one to two hours. This is due to the ketones being broken down in the rumen, although the lack of glucose available to nervous tissue to maintain normal function may be a contributing factor (Radostits et al, 2007).

Measuring the BHB levels in the blood can give a definitive answer, with a level more than 1.4mmol/ml commonly accepted as a cut-off. Blood NEFA levels can be measured to see the extent of fat mobilisation. Liver parameters, such as glutamate dehydrogenase, may demonstrate liver damage caused by fat infiltration. A liver biopsy is the definitive diagnosis for fatty liver, with following histopathology or seeing if the liver floats in copper sulphate.


Once diagnosed, a few treatment options are available, which are very similar for both fatty liver and ketosis. Any underlying/primary disease processes should be identified and treated alongside the accompanying ketosis.

The initial priority is to get the cow back on an even energy balance, or at least provide sufficient propionate (FF CaPro), so ketone bodies are not formed, nor fat is deposited in the liver.

Mono Propylene glycol

Propylene glycol in dry form (FF MPG Dry) is widely used – as, put succinctly, it increases glucose and insulin, and decreases NEFAs and BHBs (Nielsen and Ingvartsen, 2004), thus reducing the risk of ketosis and fatty liver. It serves as a glucose precursor, which is administered orally to any affected animals, with half of the propylene glycol being removed from the rumen within two hours (Clapperton and Czerkawski, 1972) via absorption, fermentation and direct passage to the intestines.

Cows receiving FF MPG Dry are known to have a higher proportion of propionate in rumen VFAs, showing there is some ruminal metabolisation (Nielsen and Ingvartsen, 2004). Propionate produces 25 adenosine triphosphate (ATP) per mole as opposed to 18 ATP per mole acetate.

Mono Propylen Glycol (MPG) in the rumen is metabolised into propionate, whereas the liver oxidises the absorbed MPG into lactate. This is converted into oxaloacetate via pyruvate and enters the Krebs cycle for gluconeogenesis. Sufficient levels of oxaloacetate are needed to prevent acetyl-CoA from entering ketogenesis (Krebs, 1966). MPG increases the amount of glucose available and increases oxidisation of acetyl-CoA. Subsequently, there will be increased insulin secretion from the pancreas, thus decreasing fat mobilisation and subsequent ketosis (Holtenius and Holtenius, 1996).

McArt et al (2012) administered 520g FF MPG Dry daily until the blood BHBs were less than 1.2mmol/L with subsequently beneficial results on milk production, displaced abomasum rates and cow survival rates. If labour is not an issue then the MPG should be continued until the animal is no longer ketotic. MPG has been shown to be beneficial to appetite due to the extra energy of the cow, although be aware that it can reduce DMI due to its unpalatability after one to two days of top dressing (Miyoshi, 2001). Therefor FF MPG Dry optionally contains red fruit flavour for increased pallatability.

The dosing guidelines must be followed strictly as FF MPG Dry at doses greater than 800g/day can lead to clinical signs such as ataxia, hypersalivation, somnolence and depression due to erythrolysis and toxicity of the CNS due to D-lactate accumulation in the brain from low levels of lactate dehydrogenase (Christopher et al, 1990). Overuse may also have deleterious effects on ruminal flora, decrease rumen motility and cause diarrhoea. FF MPG Dry contains 62% pure MPG (Mono Propylene Glycol

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