Abstract
Research in various species has indicated that diets deficient in labile methyl groups (methionine, choline, betaine, folate) produce fatty liver and links to steatosis and metabolic syndrome, but also provides evidence of the importance of labile methyl group balance to maintain normal liver function. Cats, being obligate carnivores, rely on nutrients in animal tissues and have, due to evolutionary pressure, developed several physiological and metabolic adaptations, including a number of peculiarities in protein and fat metabolism. This has led to specific and unique nutritional requirements. Adult cats require more dietary protein than omnivorous species, maintain a consistently high rate of protein oxidation and gluconeogenesis and are unable to adapt to reduced protein intake. Furthermore, cats have a higher requirement for essential amino acids and essential fatty acids. Hastened use coupled with an inability to conserve certain amino acids, including methionine, cysteine, taurine and arginine, necessitates a higher dietary intake for cats compared to most other species. Cats also seemingly require higher amounts of several B-vitamins compared to other species and are predisposed to depletion during prolonged inappetance. This carnivorous uniqueness makes cats more susceptible to hepatic lipidosis.
Highlights
Non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of metabolic syndrome, consists of a spectrum ranging from simple triacylglycerol (TAG) accumulation in the hepatocytes to steatosis with inflammation, fibrosis and cirrhosis [1]
Human and animal studies have proposed pathophysiological mechanisms for the progression of NAFLD from steatosis to steatohepatitis. These findings suggest that hepatic steatosis is related to excessive delivery of fatty acids to the liver caused by increased whole body rate of lipolysis, due to systemic insulin resistance, coupled with increased hepatic de novo lipogenesis and attenuated export of hepatic
As a result of high fatty acid uptake by the liver coupled with higher de novo lipogenesis, a higher rate of carnitine and phosphatidylcholine synthesis is required to enable fatty acid oxidation and export of very-low-density lipoproteins (VLDL), respectively
Summary
Non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of metabolic syndrome, consists of a spectrum ranging from simple triacylglycerol (TAG) accumulation in the hepatocytes (hepatic steatosis) to steatosis with inflammation (steatohepatitis), fibrosis and cirrhosis [1]. As with humans, obesity, which is becoming increasingly prevalent in cats [9], is a risk factor for feline diabetes [7,8,9,10] and feline hepatic steatosis, called feline hepatic lipidosis (FHL) [11,12,13,14] Still, despite these similarities, a thorough understanding of the peculiarities of the feline protein, one-carbon and fatty acid metabolism and their involvement in the pathophysiology of FHL is desirable if the feline model is to be pursued as a viable alternative to the use of rodents in this perspective and will be the focus of this review
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