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HOW TO FEED A DOG SUFFERING FROM HEPATIC DEFICIENCY ?

Some dietetic ranges contain products specially designed for hepatic deficiency. Canistar range does not contain any: why ?

Key points

1) There are different types and different degrees of hepatic deficiency : a single diet cannot be advisable for any kind of situation.

2) In case of moderate hepatic deficiency, the liver synthesis of proteins is frequently disturbed: then we must propose a diet that stimulates the proteic regeneration : we shall advise Canistar S2.

3) In case of very severe hepatic deficiency, sometimes the liver becomes unable to transform the by-products from the proteic metabolism (ammonia) into urea: this is the only one indication for an hypoproteic diet such as Canistar S3.

4) Fasting is an aggravating cause of hepatic deficiency, especially in cats: then we must avoid hypocaloric diets, poor in fats, that could make the appetite drop down. Provided the daily food is divided into three meals, an animal suffering from hepatic deficiency can tolerate a diet that contains at least 20 % of fat on dry matter.

The liver is the most important organ of the metabolism. In the dog, symptoms of hepatic deficiency do not show off before 75 % at least of the liver is damaged, but 8 weeks are enough to allow complete regeneration !

The food must try to facilitate the organ recuperation, to limit intoxication problems, and to prevent from malnutrition due to the accelerated consumption of endogen proteins.

The choice of a specific diet must take into account the type and the degree of hepatic deficiency, the level of serum albumin, the ideal bodyweight of the animal, its age and activity. The diet is likely to change during recovery. A single diet for hepatic deficiency is not possible. But a few main dietetic rules have to be well-known to orientate the prescription.

Proteic metabolism

The liver synthetizes undispensable proteins : serum albumins, coagulation factors ... But one of its main function is to transform the by-products of the proteic metabolism, (ammonia), into urea. At a advanced stage of hepatic deficiency, ammoniac accumulates in the blood, responsible for the apparition of nervous troubles called hepatic encephalosis.

This ammoniacal intoxication is even reinforced by the flow of proteins coming from muscular loss, that usually goes with hepatic deficiency, due to a disturbance of the hormonal balance.

The nitrogen balance is difficult to stabilize : protein intake has to be reduced to avoid the risk of ammonia intoxication, but enough proteins must be supplied to encourage muscular and hepatic regeneration.

Drastic reduction of proteins is very exceptionnally justified : i.e when there is a "short-cut" of the liver, because of an anomaly that makes portal vein and general circulation communicate (porto-systemic shunt). Then a low-protein diet, similar to those advised for renal deficiency, is well advised ; (Canistar S3).

Proteins have to be of excellent quality, highly digestible, to minimize by-products likely to produce ammonia, and other toxic compounds. We must choose sources poor in aromatic amino-acids, (offals and all-meat canned products should be avoided because of their low quality of proteins). These particular amino-acids are usable only by the liver and they can become toxic if they are not metabolized properly.

In most cases, too strict proteic restriction impairs the regeneration ability of the tissues and may dicrease the serum proteins synthesis.

Hypoproteinemia is a major indication for feeding a high-protein diet. Actually, the first goal is to help restoring the liver by an adequate protein supply, even if by-products of proteic metabolism must be still limited. A high-digestible diet, similar as for gastroenterologic diseases can be advised ; (Canistar S2).

Lipidic metabolism

Biliary salts have an emulsifying role towards dietary fats, very important for their digestion. When the secretion or the elimination of these biliary salts is disturbed (cholestasis), fats are poorly assimilated, so as for liposoluble vitamins (A, D, E, K).

However, it is dangerous to switch to a low-fat diet whose palatability is often questionable : keeping a sufficient energetic consumption must stay the priority and low-fat diets should be avoided.

Provided the daily food is divided into 3 meals at least, animals with liver disease can tolerate up to 20 % fat on dry matter.

Free fatty acids coming from adipose tissue transit through the liver before beeing released in the general circulation as lipoproteins. In case of hepatic deficiency, long chain unsaturated fatty acids (soya oil, corn oil ...) are helpful towards the liberation of fatty acids from the liver : they are part of the phospholipids that form the lipoproteins structure.

Carbohydrate metabolism

Glucose is stored in the liver under glycogen form and released according to the energetic requirements. Except very uncommon enzymatic deficiencies, this liver function is normally maintained.

As proteins must be saved for tissues synthesis, carbohydrates represent a privileged energy source, provided the starch is very well cooked and digestible.

Non-soluble vegetable fibers (ex: corn fiber) are useful for limiting proteic fermentations ; they are also able to adsorb various toxic compounds. However, it is better to use cereals meals instead of crude cereals because the crude ones depress the digestibility and they are responsible for the augmentation of by-products that have to be metabolized by the liver, already overexerted.

Let us remember that Bedlington Terrier, West Highland White Terrier, Cocker Spaniel (...), can suffer from a genetic disease that results in cupper accumulation in the liver. The treatment of this affection implies the use of cupper chelators ; dietetics alone is helpless, even if offals, rich in copper, have to be avoided in the diet.


Donated by the Borg Cardona and Co. Ltd. visit Borg Cardona website



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