SUMMARY: ROYAL CANIN Veterinary Diet^TM/MC canine HEPATIC LS 14^TM/MC is a highly palatable, digestible, low copper, modified vegetable protein diet formulated to aid the dietary management of hepatic disease in dogs.

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RATIONALE:
The liver performs many vital functions with respect to nutrient digestion and metabolism (homeostasis of blood glucose, amino acids, and trace elements), detoxification, excretion, hematology, coagulation, and hormonal balance. These functions are impaired to varying degrees in dogs with hepatic insufficiency as the result of either loss of functional tissue mass or portosystemic shunting. Nutritional support in liver disease is based on several primary factors:

--Reducing the metabolic demands placed upon the liver
--Maintaining optimal body weight and lean body mass while avoiding hepatic encephalopathy
--Overcoming nutritional deficiencies due to loss of hepatic function
--Protecting against ongoing hepatocellular damage
--Providing nutrients for hepatocyte regeneration and repair
--Minimizing inflammation, fibrosis, and complications such as ascites

HEPATIC LS 14^TM/MC is formulated to meet these objectives with modified levels of protein, carbohydrate, fiber, zinc, copper, sodium, B vitamins and antioxidants.

Protein:
The liver is the major site of protein synthesis, amino acid metabolism, and the detoxification of nitrogenous waste products. Liver disease is typically associated with reduced synthesis of serum proteins, and reduced ability to detoxify and excrete nitrogenous waste products such as ammonia. Protein malnutrition is common and manifests as weight loss, loss of muscle tissue, and hypoalbuminemia. Therefore, a sufficient supply of protein is necessary to maintain lean body mass and protein synthesis.

Excessive protein intake should be avoided as it is associated with increased production of ammonia potentially precipitating hepatic encephalopathy. A moderate reduction in protein intake is, therefore, recommended to prevent or reduce the clinical signs of hepatic encephalopathy. Furthermore, the type of protein fed can influence this risk. Poor quality proteins and meat based proteins have been suggested to exacerbate hepatic encephalopathy. Conversely, vegetable proteins such as soy protein isolate are high quality proteins containing lower concentrations of nitrogenous compounds (e.g. RNA, DNA etc). Hence, because of these virtues, soy protein isolate is recommended in liver disease.

Energy:
Hepatocellular dysfunction is accompanied by derangements in carbohydrate metabolism that result in glucose intolerance and inability to maintain blood glucose concentrations. This dysfunction can stimulate catabolism of muscle proteins for gluconeogenesis. To avoid skeletal muscle wasting, it is vital to provide sufficient energy in the form of dietary fat and carbohydrates to prevent skeletal muscle catabolism. Dietary provision of complex carbohydrates, rather than simple sugars, can be of benefit by smoothing the postprandial glycemic, response reducing insulin requirements and the glucose load presented to the liver. Carbohydrates also promote an insulin to glucagon ratio that favors an anabolic state in which amino acids absorbed from the small intestine are converted to protein rather than glucose. This also reduces the production of ammonia that accompanies the utilization of amino acids for gluconeogenesis.

Fiber:
Dietary fiber can modify the production, absorption, and elimination of ammonia and other neurotoxic microbial by-products from the large intestine. Fermentable fibers such as beet pulp and fructo-oligosaccharides (FOS) stimulate the incorporation of nitrogenous waste products into intestinal bacteria. Bacterial fermentation of fiber can also alter the colonic pH and reduce the production and absorption of ammonia. Through these dual mechanisms, fiber may reduce the risk of hepatic encephalopathy. HEPATIC LS 14^TM/MC contains a blend of soluble and insoluble fiber, and adequate dietary protein for the control of hepatic encephalopathy.

Minerals:
Zinc deficiency may occur due to poor dietary intake, reduced intestinal absorption, and increased urinary losses. Zinc is an important cofactor involved in the detoxification of ammonia via the urea cycle. Zinc deficiency may result in increased blood ammonia concentrations. Dietary zinc supplementation may inhibit collagen production in the liver and reduce hepatic fibrosis. Zinc may also protect hepatocytes from free radical injury. Most importantly, zinc inhibits the absorption of copper from the small intestine through induction of metallothionein.

Metallothionein is a protein that irreversibly chelates copper. The chelated complex is then excreted in the feces. With chronic hepatic disease, and copper storage diseases, copper accumulates within the liver. The accumulation of copper within hepatocytes initiates free radical generation, oxidative injury, and activation of collagen synthesis. The ultimate result is hepatocellular necrosis, sustained inflammation, and progressive fibrosis. Restriction of dietary copper intake, along with zinc supplementation, will reduce copper accumulation and its associated effects in dogs with chronic liver disease.

Excessive dietary sodium, particularly in patients with hypoalbuminemia or portal hypertension, can precipitate the formation of ascites. Therefore, dietary intakes of sodium should be moderate in patients with liver disease. HEPATIC LS 14^TM/MC is supplemented with zinc, enriched with antioxidants, moderately restricted in sodium, and severely restricted in copper.

Antioxidants:
There is evidence that free radicals play an important role in the pathogenesis of liver disease. Antioxidant supplementation may help to minimize hepatocellular necrosis, reduce inflammation, slow fibrosis, and, hence, minimize progression.

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REFERENCES:
Watson TDG. Nutritional management of canine liver disease. Proceedings of Waltham Symposium on liver disease. 1996; p 42-46.

Biourge V. Nutrition and Liver disease. Seminars in Veterinary Medicine and Surgery (Small Animal) 1997;12:34-44.

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