Fatty liver syndrome
By the Hybro Veterinary department - The first mention of a metabolic disease in laying hens was made 30 years ago. This disease was distinguishable by an abnormal fatty degeneration of the liver. This so-called fatty liver syndrome (FLS) has regularly been in the news since then because of the great economical significance associated with it.
The first thing that can be noticed in a flock is a increase in mortality. Birds in full production with pale heads can be found that suddenly died. Often a sharp decrease in egg production can be seen. An “affected” flock usually has a very good condition with a high bodyweight, compared with the flock's actual age and stage of production. When post mortem examination on the dead birds takes place, one finds a great deal of fat.
In particular there is an excessive amount of fat in the abdomen and in the liver. These enlarged livers are light brown to yellow in colour and have a very soft structure, due to the accumulation of fat. This degeneration of the liver can easily lead to tears in the liver capsule. As a result of this, internal haemorrhages occur which often leads to death. At the time of death, the birds are usually in the production period.
Both the amount of fat in the liver as well as the presence of haemorrhages in the liver are criteria which are often used to diagnose “fatty liver syndrome”.
Physiological background
The liver plays a very central role in the carbohydrate and fat metabolism; i.e. in converting nutrients into animal final products. It is therefore important that the absorbed carbohydrates be converted into fatty acids. In turn, these fatty acids are discharged via the blood to the ovary where the actual production of fat for the egg yolk takes place. One egg contains approximately 6 grams of fat which, for a large part, originates from the carbohydrate fraction of the feed.
The transport of fats via the blood needs some explanation. As we know, fats do not dissolve in water; this can only take place with the help of soaps, whereby the fat forms itself into small globules and is surrounded by soap molecules. When fats (and cholesterol) are carried through the watery environment of the blood, they are furnished with a special “packing material”. This is made up of phospholipids and proteins. These packed globules of fat are also known as lipoproteins.
Our knowledge of these processes is still limited. That is also why the physiological mechanism of an extreme fatty degeneration of the liver is not yet clear enough. It could be caused by a combination of:
a very high fatty acid synthesis in the liver;
a defective transport mechanism which is necessary for the discharge of these fatty acids via the blood to the various organs.
All sorts of factors advance the development of this syndrome. It is quite often difficult to tell how these influences exactly affect the metabolism of the liver on carbohydrates and fats.
Non-feed factors
It has been suggested in the past that genetical influences are important. Certain lines seem to be more sensitive than others. Even so, there is very little proof of this. However it would appear that a high potential egg production does make the layer physiologically more sensitive to FLS. A higher intensity of lay is connected with a high oestrogen activity. This hormone has a stimulating effect on the manufacture of fat in the liver.
The housing conditions of the birds also contribute towards the occurrence of FLS. This metabolic disease usually affects battery hens. The lack of space in which to move about, combined with high feed intake can stimulate fatty degeneration. It is also impossible to consume the droppings. Possible shortages of B vitamins cannot therefore be compensated.
Finally, the surrounding temperature plays an important role. FLS mainly occurs when the surrounding temperatures are high. Heat stress can overtax the metabolism so much that imbalance occurs even sooner.
Feed factors
Most of the researchers believe that the influence of feed is the primary cause of FLS. The previously mentioned factors regarding the surroundings could either strengthen or weaken the consequences of an imbalance of feed. The most important cause of FLS is the over consumption of energy, expressed as total M.E. intake per day.
It goes without saying that an excessive supply of feedstuffs over a longer period leads to an increased amount of fat. In a situation such as this, the liver must perform at its best. After all, this organ plays a key role in the metabolism of energy. In this respect, energy originating from carbohydrates is even more damaging than energy obtained from feed fat.
This may seem to be rather contradictory. It has however, definitely been proven in tests when corn was isocalorically replaced by another type of grain. A ration of corn soya showed far more FLS symptoms than a ration of wheat soya.
In order to keep the energy content of both feeds the same, a percentage of fat was added to the wheat feed. The differences in the fatty degeneration of the liver is therefore not only caused by the influences of a type of grain but the relationship between carbohydrate and fat energy in the feed. The positive influence of feed fat can even be strengthened if the percentage of unsaturated fatty acids is relatively high. Linoleic acid is especially valuable.
Soya oil, sunflower oil and corn oil are therefore preferable to fat sources which have a more saturated character. Bearing this in mind, it is advisable to give feed with extra soya oil when there are cases of fatty liver syndrome.
Damage to the liver, i.e. fatty degeneration can also be caused by the presence of poisonous elements in the feed. Toxines arising from moulds (aflatoxine in particular) can be very damaging. Eruca acid which comes from rape seed products can cause degeneration of the liver.
An important point is to know the effects which vitamins and so-called lipotropes can have when present in feed. These lipotropes are needed to produce phospholipids in the liver. As already stated, these phospholipids are very important as "packing material" when fatty acids from the liver are discharged to the various organs. The vitamins, the B group in particular, fulfil many functions in metabolising carbohydrates and fats. In literature there is unfortunately a lot of disagreement as to how much FLS influences both categories. However, these elements are often successfully applied when controlling metabolic diseases.
Prevention and therapy
From what we have already learned, some preventive measures can in principle, be concluded. Factors which stimulate FLS should be avoided as much as possible. In practice though, it is often difficult to achieve this.
One important cause, energetic over consumption does offer some possibilities. Decreasing the daily ME intake by means of feed restriction and/or reducing the ME value of the feed can be considered. This is certainly possible when fighting FLS. The feed composition can also be adjusted. If the carbohydrate content is decreased by means of increasing the amount of fat which is rich in linoleic acid, the ration will become less sensitive to FLS.
Apart from these general measures, a number of specific actions can be taken in order to optimise the functioning of the liver. This particularly concerns the application of lipotropes and increasing certain vitamins. The following "raw materials" can be used for the synthesis of phospholipids:
lecithin
choline
inositol
betaine
methionine
Quite a number of important phospholipids are already present in lecithin. That is why the addition of a few percent of lecithin is often advised. Another advantage is that lecithin somehow curbs the appetite which is useful in the fight against over consumption.
Methionine and betaine are actually forerunners of choline. Vitamins B12 and pholium acid stimulate the conversion to choline. It is also known that Vitamin B1 and Biotine have an essential function in the metabolism of carbohydrates. It is this metabolism which runs at full speed. If problems occur it is a good idea to check the supply of Vitamin B1 and Biotine.
Finally, it has always been thought that Vitamin E (possibly in combination with selenium) has a positive effect on the synthesis and the transport of fats.
Summary and conclusions
Fatty liver syndrome (FLS) in poultry is a metabolic disease of economical significance.
Knowledge of the physiological processes in the liver connected with this disease is still limited.
A great number of factors influence the development of FLS. These include both feed as well as climate/housing conditions.
Alteration of the energy intake and feed composition can help to fight or even prevent FLS.
Source: Hybro B.V. - March 2005