Royal Canin Nutritional Information

Royal Canin Nutritional Information

Focus on: Vitamin B12 (cobalamin)

Definition and origins

The anti-anemic qualities of calf liver were first discovered in 1925. They were linked to the existence of an "extrinsic dietary factor", which was only isolated mid-century. Given the name vitamin B12 or cobalamin, this substance is mainly found in animal products (fish, meat and offal). Whatever the source, vitamin B12 is always synthesized by microorganisms. It is very stable during the heat treatment of food products.

Formula

Vitamin B12 is the only vitamin to incorporate a mineral element in its chemical formula, namely cobalt.

The molecule’s nucleus is a tetrapyrrole with a central cobalt atom, linked to 4 pyrrolic nitrogen atoms, 1 ribonucleotide and 1 anionic ligand (X). There are several types of cobalamin, depending on the nature of the ligand, including:

X = CN (cyanide): cyanocobalamin

X = CH3 (methyl): methylcobalamin

X = OH (hydroxyl): hydroxocobalamin

X = 5’dAd (5’deoxyadenosyl): adenosylcobalamin

In cats, cobalamin is mainly found in the form of hydroxocobalamin and adenosyl cobalamin.

Biological Roles

Cobalamin plays an essential role in the synthesis of nucleic acids (in synergy with folic acid). A deficiency disrupts protein synthesis, especially for fast-regenerating tissues like hematopoietic tissue.

Risk of Vitamin B12 Deficiency in Cats

A fall in the body’s cobalamin reserves is seen in cats suffering from pancreatic or hepatic disease.

The depletion of reserves may be explained by chronic dysorexia or intestinal malabsorption reducing the quantity of cobalamin available to the animal. The deficiency may also be secondary to an insufficiency of intrinsic factor essential to the absorption of cobalamin. In cats, this glycoprotein is synthesized only by the pancreas, so pancreatic disease is a risk factor for deficiency. Any imbalance in the intestinal bacterial flora is also likely to reduce the absorption of cobalamin, as intestinal bacteria use vitamin B12 and may also form connections to intrinsic factor.

Cobalamin Supplementation

Cats are not able to store large quantities of cobalamin in the body and quickly become deficient when their homeostasis is disrupted. Supplementation of vitamin B12 is essential in the event of pancreatic or hepatic disease. It is also indicated when an underlying intestinal disease is suspected. Because of the above assimilation problems, oral supplementation is ineffective, so parenteral administration is required.

Figure 27. Vitamin B12.

The plasma concentration of cobalamin should be measured prior to initiating supplementation. It is generally recommended to first administer 250 - 500 μg/kg (on average 1000 μg / cat) SC. Depending on the cobalamin plasma concentration, this dose may be repeated every two to three weeks until the plasma cobalamin concentation normalizes. The benefit of long-term supplementation should be evaluated on the basis of the underlying disease and the response to treatment.

The potential toxicity of large cobalamin doses administered to cats has not been addressed in any publications.

Feline Idiopathic Hepatic Lipidosis

Epidemiology

Cats suffering from hepatic lipidosis are generally aged 4 - 12 years. No particular breed appears to be predisposed, but IHL is most common in neutered cats.

Feline hepatic lipidosis is characterized by the excessive accumulation of hepatic lipids (triglycerides). When associated with other pathologies (e.g. diabetes mellitus, renal insufficiency, chronic enteritis) it is qualified as secondary, otherwise it is known as idiopathic hepatic lipdosis (IHL). (© Yves Lanceau/Royal Canin).

Most cases of IHL are observed after prolonged fasting (4 - 7 weeks) in cats that were previously obese, although most have already lost at least 30% of their body weight by the time they are taken to the veterinarian. The trigger for anorexia is yet to be identified. Stress factors that should be considered are moving, vacation, arrival of another cat or a baby in the home and poorly palatable food. IHL is said to be more common in cats that live in a group than in those that live alone. IHL "epidemics" are not uncommon in cat colonies in the event of a change of environment or food.

Pathophysiology

Contrary to the process in humans, obesity does not lead to hepatic lipidosis in cats. Some endocrine and/or nutritional imbalances – diabetes mellitus, hyperthyroidism, choline and essential amino acid deficiency, energy overdose during parenteral feeding and a severe diet – do however induce lipidosis in cats. In these situations, lipidosis is generally moderate and does not lead to clinical signs.

The pathophysiological mechanisms responsible for the accumulation of hepatic lipids during prolonged fasting in cats have not yet been fully described (Figure 28). This observation constitutes a metabolic particularity in cats, as fasting and hepatic lipidosis are not associated in humans, dogs or rats. In cats, the lipids accumulate from the beginning of the period of fasting (Figure 29), but the clinical [anorexia, muscular atrophy] and biochemical signs [elevated hepatic enzymes and serum bilirubin (Figure 30)] only appear when the lipidosis becomes very severe.

Figure 28. Pathophysiological mechanisms involved in hepatic lipidosis.

Figure 29. Hepatic biopsies (as seen with an electronic microscope).

Figure 30. Hyperbilirubinemia visible. The color of the serum changes abruptly during hepatic lipidosis: the transformation occurs approximately 3 weeks after the onset of the rise in alkaline phosphatase.

A preliminary work suggests that cats are not able to efficiently save protein during prolonged fasting. It is therefore possible that the deficiency of one or more indispensable amino acids causes dysfunction in hepatic lipid metabolism, leading to pathological lipidosis.

These observations suggest prudence with respect to a low-calorie diet for cats. Veterinarians must advise owners to make sure their cat actually consumes the recommended food. In case of doubt, the measurement of alkaline phosphatase in the serum can be used as a marker of hepatic lipidosis (Figure 31).

Figure 31. Serum concentrations of alkaline phosphatase.

Dietary Recommendations

Aggressive nutritional support is the treatment of choice. Our own observations as well as those of other authors show that a highly digestible complete food that respects the following nutritional balances would appear to be appropriate:
- 30 - 50% calories from protein
- 35 - 50% calories from fat
- 20 - 30% calories from carbohydrate

Cats with IHL are glucose-intolerant and preparations rich in rapidly assimilated carbohydrates present a risk of hyperglycemia. In the event of hepatic encephalopathy, limiting the protein content to 20 - 25% of calories is recommended.

The supplementation of certain nutrients (choline, arginine, citrulline, taurine, thiamine, vitamin C and zinc) has been recommended for the nutritional treatment of IHL. The efficacy of these supplements has not been scientifically demonstrated.

A properly balanced nutritional diet will reduce the bilirubin and the serum hepatic enzymes within 1 - 2 weeks. They typically return to physiological levels within 4 weeks. Most cats accept food after 2 - 3 weeks of enteral feeding. The liver regains its normal histological structure within 4 - 8 weeks.

Feeding Practice

The treatment of hepatic lipidosis demands constant attention of the veterinarian. It is not uncommon for the clinical signs to appear to worsen at the start of treatment. It is important to monitor the potassium concentration and reintroduce the cat to food very gradually.

Type of Food

Cats with IHL require assisted feeding. A nasoesophageal enteral feeding tube is a cost-effective, rapid and safe way to administer liquid nutrition or wet food homogenized with water. Tube placement requires local anesthesia without expensive equipment. In our experience, it does not prevent cats from eating normally. If the food is not liquid enough, nutritional assistance may be provided via the placement of a gastric or esophageal enteral feeding tube.

It is vital that the cat continues to be fed through vomiting or diarrhea, which are both common during the first week. If the digestive problems are uncontrollable, temporary parenteral feeding may be initiated.

Rationing

During the first day of hospitalization, it is recommended to feed the cat four times at intervals of at least three hours and to limit the serving to 25 mL. Over the following days, increase the serving by multiples of 5 mL until the cat is consuming 60 kcal/kg body weight/day. This will generally be achieved within 5 - 7 days. Increasing the serving very gradually limits vomiting and diarrhea. After ten days, meal frequency should be reduced to three times per day. If given time to adapt, cats will comfortably tolerate up to 120 ml per serving.

Preventing Food Aversion

Cats are likely to refuse to eat a food they associate with digestive disorders (nausea, vomiting) that appear during the consumption period. This type of food aversion appears to be a major component in the anorexia associated with hepatic lipidosis.

Recommendations to Reduce the Risk of Food Aversion:

• Do not offer multiple types of food to confirm the anorexia
• Use exclusively a feeding tube throughout the period of assisted feeding during the first 10 - 15 days of treatment
• After 10 - 15 days of treatment, propose a diet that the cat has not consumed since it has been sick. Don't insist if the cat does not eat immediatly. Repeat the operation after 48 hours until the cat feels like eating spontaneously.

Conclusion

The prognosis of IHL has greatly improved since the recognition of the importance of nutritional support in its treatment. It is nevertheless more reserved when the hepatic lipidosis is complicated by another underlying disease (e.g. chronic gastroenteritis, chronic kidney disease etc.).