Poor nutrition is a common finding in patients with chronic hepatobiliary disease. A proper nutrition is in fact crucial for the uptake of the main hepatotrophic factors, which include several hormones (insulin, glucagon, parathyroid hormone, glucocorticoids, thyroid hormones, etc.). It is worth recalling that, unlike many mature cells, hepatocytesretain their ability to regenerate even in their adult stage; the nutritional management of hepatobiliary disease must take this factor into consideration and use it to its advantage.
VASCULAR ANOMALIES: PORTOSYSTEMIC SHUNT
In the presence of portosystemic shunts nutritional management is important, particularly in young patients with stunted growth. The diet must be highly digestible, highly palatable, and contain proteins of high biological value, essential fatty acids, minerals and vitamins. Proteins derived from milk and vegetables are generally preferred, in view of their low content of aromatic amino acids (tyrosine and phenylalanine) and high content of branched-chain amino acids (isoleucine, leucine and valine). Protein contents of 18-22% DM in the dog and of 30-35% DM in the cat should not be exceeded (Tobias K.M., 2009). In the presence of hepatic encephalopathy, a low-protein diet is instead necessary (protein content of around 15% DM in the dog and <20-25% DM in the cat), in combination with medical treatment, in order to reduce the production of ammonia and microbial absorption. A moderate amount of soluble fibre is necessary for the regulation of the gut flora (total fibre of about 3-8% DM). The protein intake may be increased once the neurological symptoms have been resolved, but this must be done carefully and with a slow progression, at intervals of 1-2 weeks. Supportive therapy with nutraceuticals is recommended in various liver diseases, however if vascular anomalies can be corrected surgically this is not necessary. Nutraceuticals are instead fundamental in portosystemic shunts in which surgical correction is not an alternative; these cases require the administration of: SAMe (S-adenosyl-L-methionine), in view of its hepatoprotective, antioxidant and anti-inflammatory effect; Vitamin E, an antioxidant and an inhibitor of lipid peroxidation; Silymarin, derived from the achenes of milk thistle (Silybum marianum) (Fig. 1), which is an inhibitor of lipid peroxidation of hepatocytes and of microsomal membranes, with a protective effect against the genetic damage resulting from the suppression of hydrogen peroxidase, superoxide and lipoxidase and is in addition capable of increasing glutathione content, with a resulting hepatoprotective effect; ursodeoxycholic acid, with its anti-inflammatory, immunomodulatory and antifibrotic properties (Tobias K.M., 2009).
CHRONIC HEPATITIS IN THE DOG
In dogs with chronic hepatitis proper nutritional management is fundamental and should aim at maintaining an adequate body condition in order to favour liver regeneration while reducing clinical signs in case of hepatic encephalopathy (HE). Protein intake should be between 17 and 20% of the metabolic energy requirement and the proteins must be highly digestible and of high biological value. Protein restriction is required only in the presence of HE. The dietary fibre used must be both soluble, to decrease the absorption of NH4 +, and insoluble, to normalize food transition time and prevent constipation and the absorption of toxins. The diet must also contain an increased level of zinc and an adequate content of antioxidant agents. Zinc acetate supplementation can be helpful for its antioxidant and antifibrotic properties; it has also been described as being able to reduce the severity of HE.
METAL-INDUCED HEPATOXICITY
Thenutritional management of iron-induced hepatotoxicity is based on the use of antioxidants (vitamin E and silymarin) and of thiol donors, as iron accumulation in the liveris often associated with vitamin E deficiency and with a reduced GSH/GSSG tissue balance (Fig. 2). Copper-induced toxicity requires instead the use of specific chelating agents for 2-4 months, among which D-Penicillamine or Zinc acetate, and a diet with reduced copper intake, increased zinc and with an adequate level of high quality proteins (Brewer G.J. etal., 1992). The inflammatory component of metal-induced hepatotoxicity may be reduced with the supplementation of omega-3 fatty acids; however, the specific dosages effective in dogs and cats have not yet been reported.
FELINE HEPATIC LIPIDOSIS
In the medical treatment of cats with hepatic lipidosis the basis for success consists in providing an adequate nutritional support. An adequate supplementation of energy is needed to prevent protein breakdown, inhibit peripheral lipolysis and avoid the excessive consumption of energy, which promotes the accumulation of liver triglycerides. Hospitalization of the patient is usually necessary to allow the forced feeding of a high energy (4.2 kcal ME/g DM) and high protein (30-45% DM) diet by means of a feeding tube for 7-10 days (Fig. 2) or until resumption of voluntary feeding. The protein and amino acid deficit may cause hepatic lipid accumulation, with inhibition of the synthesis of the lipoproteins necessary for normal metabolism and lipid transport (Biourge et al., 1994a; Biourge et al., 1994b). Protein supplementation, increased by a quarter of the normal daily requirement (22g/day), has been shown to significantly reduce the accumulation of lipids in the liver and promote the urea cycle during prolonged fasting in obese cats (Biourge et al., 1994b).
In cats with hepatic lipidosis the supplementation of arginine, taurine and L-carnitine is also essential. L-carnitine (250-500 mg/day) stimulates the beta-oxidation of fatty acids by the hepatocytes (Blanchard G. et al., 2002), while taurine (> 0.3% DM) is recommended as it is an amino acid which can increase the water solubility of bile acids, reduce cellular toxicity and facilitate renal circulation and elimination (Center S.A., 2005). The level of arginine in the diet should always be maintained between 1.5 and 2% DM (NRC, 2006), so as to compensate for the deficit present in cats with hepatic lipidosis during hyperammonaemia and hepatic encephalopathy.
In addition, cats with hepatic lipidosis may also develop hypokalaemia due to inadequate bowel absorption, vomiting, polydipsia and polyuria, magnesium depletion and concomitant chronic renal failure (Center et al., 1993). In accordance with such study, the dietary intake of potassium may be increased to 0.8-1% DM.
Suggested reading
- Armstrong PJ, Blanchard G. Hepatic Lipidosis in Cats. Vet Clin Small Anim 2009;39:599–616.
- Biourge V, Groff JM, Morris JG, Rogers QR, et al. Long-term voluntary fasting in adult obese cats: nitrogen balance, plasma amino acid concentrations and urinary orotic acid excretion. Journal of Nutrition 1994;124(12 Suppl):2680S-2682S.
- Biourge VC, Massat B, Groff JM, Morris JG, Rogers QR, et al. Effects of protein, lipid, or carbohydrate supplementation on hepatic lipid accumulation during rapid weight loss in obese cats. American Journal of Veterinary Research 1994;55(10):1406-15.
- Blanchard G, et al. Dietary L-carnitine supplementation in obese cats alters carnitine metabolism and decreases ketosis during fasting and induced hepatic lipidosis. J Nutr 2002;132:204-210.
- Brewer GJ, Dick RD, Schall W. Use of zinc acetate to treat copper toxicosis in dogs. Journal of American Veterinary Medical Association 1992;201:564-568.
- Center SA, et al. A retrospective study of cats (n = 77) with severe hepatic lipidosis (1975-1990). J Vet Intern Med 1993;7:349-359.
- Center SA. Feline hepatic lipidosis. Vet Clin North Am Small Anim Pract 2005;35:225-269.
- National Research Council (NRC). Nutrient Requirements of Dogs and Cats. Washington DC: National Academies Press 2006.
- Tobias KM. Portosystemic shunts. In: Bonagura JD, Twedt DC, ed. Current veterinary therapy XIV, ed 14. St Louis: Saunders; 2009.