Nutritional requirements and starvation in healthy cats

The cat is not a small dog especially with respect to critical care medicine. The physiologic response to shock, the procedures required for resuscitation, and the parameters that require careful monitoring present specific challenges that are unique for the critically ill cat. Although some feline disorders cause an increased appetite (diabetes mellitus or hyperthyroidism), the majority of feline illnesses result in partial or total anorexia.

Isabelle GOY-THOLLOT
DVM, MSc, PhD

Isabelle Goy-Thollot graduated from Maisons-Alfort’s École Nationale Vétérinaire in 1989. She was a medical intern at Maisons-Alfort between 1989 and 1991, specializing in companion animals. She co-founded the SIAMU, the critical care, anaesthesia and emergency medicine unit at Lyon’s École Nationale Vétérinaire in 2000. She currently leads the SIAMU as well as being in charge of instruction in emergencies and critical care for companion animals. Isabelle has been President of the European Veterinary Emergency and Critical Care Society (EVECCS) since 2005. She is a member of the scientific committees of various journals and veterinary associations in France. Isabelle has developed her expertise in various placements in Utrecht (Netherlands) and Davis (USA) as well as participating in many activities for journals and conferences.

Denise A. ELLIOTT
BVSc (Hons) PhD Dipl. ACVIM, Dipl. ACVN

Denise Elliott graduated from the University of Melbourne with a Bachelor in Veterinary Science with Honors in 1991. After completing an internship in Small Animal Medicine and Surgery at the University of Pennsylvania, Denise moved to the University of California-Davis where she completed a residency in Small Animal Internal Medicine, a fellowship in Renal Medicine and Hemodialysis, and a residency in Small Animal Clinical Nutrition. Denise received board certification with the American College of Veterinary Internal Medicine in 1996 and with the American College of Veterinary Nutrition in 2001. The University of California-Davis awarded a PhD in Nutrition in 2001 for her work on Multifrequency Bioelectrical Impedance Analysis in Healthy Cats and Dogs. Denise is currently the Director of Scientific Affairs for Royal Canin USA.

Introduction

With the emphasis in first diagnosing the underlying disease process, nutrition is often relegated as a late therapeutic process, typically considered when the patient has already been hospitalized for 4-5 days and has received little to no nutritional support. Moreover, a common practice is to wait just one more day, whereby there is some unreasonable expectation that anorexia that persisted for days will simply reverse itself because intravenous (IV) fluids have been administered. In reality, loss of appetite is one of the most powerful and long lasting features of severe disease. Therefore, the correct assumption should be that appetite will not resolve with supportive care and timely nutritional intervention should be implemented.

As more and more research uncovers the benefits of enteral nutrition and the complications that are derived from gut atrophy, critical care human specialists now feed patients much earlier than before in the disease process. This practice has resulted in improved outcomes and fewer complications. In veterinary medicine a similar transition has begun over the last few years, and is gaining momementum.

The two approaches to feeding critically ill cats are:

• enteral feeding, in which some portion of the gastrointestinal tract is utilized
• and parenteral feeding, in which nutrients are administered in a manner other than using the gastrointestinal tract, most commonly via central or peripheral venous access.

In the past several years, transitioning from ineffective strategies such as force- or syringe-feeding, warming foods, and adding flavor enhancers, to more recent recommendations for early tube feeding, novel methods of administrating nutrition to critically ill cats have resulted in increased survival rates.

1. Nutritional Requirements and Starvation in Healthy Cats

Specific Requirements

Cats Are Carnivores

Carnivorous by nature, cats require few carbohydrates but need high levels of protein. Adult cats require two to three times more dietary protein than omnivorous species, and have a high requirement for essential amino acids as energy sources (Zoran, 2002). Unable to adapt their urea cycle enzymes or aminotransferases to reduced protein intake, cats possess limited ability to adjust protein metabolic pathways for conserving nitrogen. Feline metabolism mandates cats to use protein for maintenance of blood glucose concentrations even when sources of protein in the diet are limited. These peculiarities help to explain the rapid onset of protein malnutrition in anorectic cats (Zoran, 2002; Center 2005) (Figure 1).

Figure 1. Nitrogen balance in a critically ill cat and in a healthy cat.

Hastened use coupled with an inability to conserve or synthesize certain amino acids, necessitates a higher dietary amino acid intake for cats compared with most other species (Kerl & Johnson, 2004; Kirby, 2004; Center, 2005).

• Taurine deficiency has been proven to cause dilated cardiomyopathy, reproductive disorders and retinal degeneration.
• Arginine has important roles in nitrogen elimination and the urea cycle in addition to stimulating endocrine secretagogue activity, improving nitrogen retention, reducing nitrogen loss in post-operative patients, enhancing collagen deposition in wounds, enhancing T-cell function, and growth of lymphocytes (Morris & Rogers, 1978; Barbul & Hurson, 1994; Zoran, 2002; Center, 2005; Saker, 2006). Arginine is also a precursor of nitric oxide (NO) (Barbul & Hurson 1994).
• Methionine and cysteine are key methyl group donors important for the production of many metabolites such as glutathione, which is an important antioxidant and scavenger of free radicals (Zoran, 2002; Center, 2005).
• The amino acid glutamine (GLN) has been described as a "conditionally essential amino acid". Increased demand coupled with poor supply in critical patients may result in compromise of the gut mucosal barrier, with subsequent bacterial translocation and systemic infection. Impairment of reticuloendothelial function, in conjunction with a reduction in antibody production increases the risk of sepsis and multiple organ failure (Elliott & Biourge, 2006). Glutamine also has an important role in acid-base balance. Plasma glutamine levels have been reported to decrease by 58% after critical illness or injury, to remain decreased for up to 3 weeks and was associated with increased mortality in critically ill patients (Wischmeyer, 2003).

Cats Need Minimal Amounts of Carbohydrates

Cats have several physiologic adaptations that reflect their low carbohydrate intake. Cats lack salivary amylase, the enzyme responsible for initiating starch digestion. Cats also have low activities of intestinal and pancreatic amylase and reduced activities of intestinal disaccharidases that digest carbohydrates in the small intestine. These species specific differences however, do not mean that cats cannot use starch. In fact, cats are extremely efficient in their use of digestible carbohydrates. Cats also have minimal activity of hepatic glucokinase and glycogen synthetase probably as a result of a metabolism designed to use gluconeogenic amino acids and fat, rather than starch. As a result, cats have limited ability to rapidly minimize hyperglycemia from a large dietary glucose load (Zoran, 2002).

High levels of dietary carbohydrates may also decrease protein digestibility in cats. This is due to a combination of factors, including increased passage rate. Increased amounts of carbohydrates in diets also results in increased microbial fermentation in the colon and increased production of organic acids (Kienzle, 1994).

Cats Have a Specific Requirement for Polyunsaturated Fatty Acids

Fat typically provides most of the fuel for energy. Essential fatty acids (EFAs) for cats include linoleic, linolenic, arachidonic, eicosapentaenoic and docosahexaenoic acid. Most species can convert linoleic acid to arachidonic acid, the primary precursor for the 2-series prostaglandins, leukotrienes and thromboxanes. Arachidonic acid is required for maintenance of cell wall and tissue integrity and can be found in diets containing animal sources of fats. Cats however, do not have the enzymatic machinery (lack adequate hepatic Δ-6-desaturase activity and other hepatic desaturases) to synthesize derivatives of arachidonic acid (Zoran, 2002). Therefore arachidonic acid is an essential nutrient needed in the feline diet (Kirby, 2004).

Vitamin Needs of Cats Are Unique

Cats require higher amounts of several water soluble B-vitamins including niacin, thiamine and pyridoxine compared with other species, and are predisposed to depletion during prolonged starvation. In addition, in some disease states, cats also require additional supplementation with cobalamin (B12) (Zoran, 2002; Kirby, 2004).

Cats do not have the ability to convert beta-carotene to active vitamin A (retinol). Cats lack dioxygenase enzymes in the intestinal mucosa that split the beta-carotene molecule to vitamin A aldehyde (retinal). Therefore, preformed vitamin A must be supplied in the diet. Vitamins E and K are also important and may become deficient in cats that have prolonged anorexia (Zoran, 2002).

Effect of Fasting and Starvation in Healthy Cats

The normal nutrient-metabolism cycle in healthy animals involves an alternating system of feeding and fasting. In the fed state, the hormonal response to the nutrients glucose and amino acids, is stimulation of insulin secretion coupled with a reduction of glucagon secretion (substrate control) (Table 1). This results in stimulation of glycogenesis and repletion of the glycogen reserves, an increase in protein synthesis and the storage of fats. During the fasted state, plasma levels of glucose and amino acids fall, insulin secretion is reduced and glucagon secretion is increased which stimulates gluconeogenesis and glycogenolysis.

Periods of fasting longer than three to five days induces a state of starvation. In this situation, there is a further reduction in insulin levels and an increase in glucagon secretion. In addition, mild sympathic activation stimulates hormone-sensitive lipoprotein lipase which increases the release of free fatty acids (FFAs) from adipose tissue. Excess FFAs are converted by the liver to ketone bodies, which substitute for glucose as energy substrates in the brain and other organs. Ketones help to decrease skeletal muscle breakdown and amino acid release by reducing the obligatory demand for glucose, and gluconeogenesis. With chronic starvation, glucagon levels return to their post absorptive levels and catecholamine levels decrease. The basal metabolic rate decreases due to a reduction in the peripheral conversion of thyroxine (T4) to triiodothyronine (T3) (Atkinson & Worthley, 2003).

In carnivores such as cats, glycogen stores are quickly depleted and this leads to the initial mobilization of amino acids from muscle stores. Within days, a metabolic shift occurs toward the preferential use of fat deposits, which spares the catabolic effects on lean muscle tissue (Chan, 2006; Chan & Freeman, 2006) (Figure 1).