The underlying problem in a lipidotic cat is their dysfunctional lipoprotein and lipid metabolism, particularly in the transport and accumulation of VLDL (very low density lipoprotein).i.e., fatty acids. If HE is present, then lactulose (0.25-2 ml/kg to effecting soft stools), plus metronidazole (7.5 mg/kg PO q12h) are indicated. Protein restriction should only be considered in the cat with hepatic encephalopathy (uncommon). Cage resting cats with HL may reduce muscle release of ammonia, thus may be beneficial. Arginine is needed for normal detoxification of nitrogen. Arginine is an essential amino acid in the cat (easy to remember: Carnitine-Arginine-Taurine = CAT). Don't use carbohydrates instead of fat, as these cats are already prone to insulin resistance. Protein is essential for this process, in order to make lipoproteins VLDL, thus protein restriction is contra-indicated unless encephalopathy is present.įeeding a minimum of 50 kcal/kg ideal body weight/day of a good quality, calorie dense diet is essential. This fuels the already imbalanced TG dispersal mechanisms. While fat may become depleted on the limbs and dorsal trunk, abdominal and thoracic fat stores remain spared.įat depletion dorsally with abdominal and thoracic fat sparedĭiagnosis and treatment RULE #1 with yellow cats: - FEED FIRST, DIAGNOSE LATER! - Lack of nutrients promotes lipolysis and glycogenolysis. Domestic shorthair cats are breed predisposed this finding could be a reflection of this breed's greater incidence in the population.Ĭlients bring their cat in because of weight loss or anorexia, vomiting, lethargy and weakness. Cats of any age may be affected most commonly cats are between 4-15 years of age. Obese female cats are at greatest risk of developing hepatic lipidosis. Given the complexity of lipid metabolism, it is, however, unlikely that one pathogenesis explains HL in all affected individuals. An imbalance between essential lipoprotein components will also interfere with fat dispersal. Therefore, in these cats, lipidosis may reflect the liver's inability to match fat dispersal with delivery from systemic sources. Unrestricted release of fatty acids from excessive adipose fat promotes lipidosis because up to one third of mobilized fat may be residing in the liver at one time. For example, any systemically ill person is expected to have some fat vacuoles in their hepatocytes. It is believed that the lipid accumulation reflects an underlying metabolic disorder. The development of lipid vacuoles within hepatocytes does not directly have a noxious effect on the cell. They accumulate in the liver when the rate of hepatic synthesis exceeds their dispersal. Lipid vacuolation in lipidosis is predominantly composed of triglycerides. Many cats developing hepatic lipidosis (HL) are obese.įat in the liver is of five types: triglycerides (TG), phospholipids, lipoproteins, cholesterol and cholesterol esters. A previously obese individual undergoing starvation is at increased risk for lipolysis. Regulation of fat metabolism in the adipocyte is modulated by blood glucose concentration as well as hormonal, neural and pharmacological mechanisms.
0 Comments
Leave a Reply. |
Details
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |