Summary of the article: https://doi.org/10.1016/j.cvsm.2025.03.007

Hepatobiliary diseases in dogs and cats generate profound metabolic disturbances affecting digestion, detoxification, protein synthesis and energy regulation. Nutritional management is a critical component of treatment, directly influencing clinical progression, hepatic regeneration and the prevention of associated complications. This summary compiles the essential points needed to understand how nutrition modulates physiological responses across different hepatic conditions.

General considerations in severe liver disease

Patients with significant hepatic dysfunction experience metabolic changes that alter the utilisation of energy, proteins, fats and micronutrients. Preventing catabolism and supporting residual liver function are central objectives.

Key points

• Anorexia and dysrexia are common and compromise energy intake.
• Muscle catabolism accelerates, promoting loss of lean mass.
• Hyperglucagonaemia and insulin resistance may disrupt glucose homeostasis.
• Glycogen stores deplete rapidly, increasing reliance on amino acids for gluconeogenesis.
• Correcting the energy deficit is essential to prevent hepatic lipidosis, particularly in cats.

Energy: the primary priority in critical patients

Insufficient energy intake is one of the most detrimental factors in the progression of liver disease. Malnutrition affects immunity, wound healing and hepatic regenerative capacity.

Key points

• The initial target is meeting the RER, adjusting according to weight and body condition.
• Assisted feeding is essential in feline hepatic lipidosis.
• Hypermetabolic states may arise in advanced disease, increasing energy needs.
• Rapid glycogen depletion promotes muscle breakdown to sustain gluconeogenesis.

Protein and amino acids: balancing need and tolerance

The liver regulates plasma protein synthesis, coagulation factor production and amino acid metabolism. Protein intake must be adapted according to the presence or absence of hepatic encephalopathy.

Key points

• Protein restriction is only justified when encephalopathy is present.
• In the absence of encephalopathy, many patients require increased protein, not reduced.
• Vegetable, dairy and egg proteins reduce ammonia and purine load.
• The balance between branched-chain and aromatic amino acids influences neurological tolerance.
• Protein tolerance varies between individuals and must be adjusted gradually.

Table 1. Recommended protein sources according to neurological tolerance

Fats and lipid metabolism

The liver is central to lipoprotein synthesis and degradation, bile production and fatty acid oxidation. Dietary fat may be beneficial or detrimental depending on the hepatic condition.

Key points

• High-fat diets improve palatability and energy intake in patients with poor appetite.
• Fat supports absorption of fat-soluble vitamins, often deficient in severe disease.
• Excess fat may worsen signs in cholestasis or gallbladder mucocele.
• Hyperlipidaemia and pancreatitis require moderated fat intake.

Vitamins, minerals and antioxidants

Hepatic disease affects the availability and metabolism of multiple micronutrients. Supplementation must be precise and tailored to the clinical picture.

Key points

• Fat-soluble vitamins may be reduced due to malabsorption or cholestasis.
• Vitamin E is useful in conditions with high oxidative stress.
• Vitamin K may be required in cases of dysbiosis or coagulation abnormalities.
• Zinc reduces oxidative stress and limits copper absorption.
• SAMe and silybin provide hepatoprotective and antioxidant benefits.

Table 2. Key micronutrients in hepatic disease

Hepatic encephalopathy and portosystemic shunts

Hepatic encephalopathy requires specific nutritional strategies to reduce ammonia production and absorption, as well as other neurotoxic compounds.

Key points

• Protein should be provided at the highest tolerated level without inducing neurological signs.
• Vegetable, dairy and egg proteins are preferred.
• Feeding should be divided into multiple small meals.
• Soluble fibre helps reduce postprandial ammonia peaks.
• Lactulose reduces ammonia absorption by acidifying the colon and accelerating transit.
• Purine control is essential to prevent urate formation in patients with shunts.

Feline hepatic lipidosis

Hepatic lipidosis is a nutritional emergency in cats. Reversing the catabolic state is the primary objective.

Key points

• Assisted feeding is required in most cases.
• Gradual increases in intake prevent refeeding syndrome.
• Veterinary liquid diets are preferable to human formulas.
• Diets lacking arginine must be avoided to prevent hyperammonaemia.
• Electrolytes (K, Mg, P) must be monitored during refeeding.

Copper-associated hepatitis

Copper accumulation in hepatocytes causes oxidative stress and chronic inflammation. Dietary management is essential to reduce copper load.

Key points

• Certain breeds have genetic predisposition.
• Reducing dietary copper is fundamental to controlling progression.
• Zinc enhances intestinal copper excretion.
• Chelation combined with low-copper diets is the most effective approach.
• Hepatic diets typically contain reduced copper levels.

Therapeutic hepatic diets

Hepatic diets are not required in all cases but are valuable in specific pathologies.

Key points

• Indicated in encephalopathy, urate issues and copper-associated hepatitis.
• Renal diets may be useful in encephalopathy due to lower protein load.
• No specific hepatic diets exist for cats; renal diets are adapted instead.
• Fresh food additions should not exceed 10% of daily energy intake.

Conclusion

Nutritional management of hepatobiliary diseases in dogs and cats requires an individualised strategy that considers pathophysiology, protein tolerance, energy status and associated metabolic disturbances. Nutrition directly influences clinical progression, hepatic regeneration and the prevention of complications such as encephalopathy, lipidosis or copper accumulation. Appropriate protein sources, controlled fat intake, targeted micronutrient supplementation and the use of therapeutic diets are key tools to optimise treatment outcomes.