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Feline hepatic lipidosis, also known as feline fatty liver syndrome, is one of the most common forms of liver disease of cats. [1] The disease officially has no known cause, though obesity is known to increase the risk. [2] The disease begins when the cat stops eating from a loss of appetite, forcing the liver to convert body fat into usable ...
The most commonly noticed change in serum chemistry is a non-major increase in liver enzymes. More than 90% of hyperthyroid cats have an increase in either serum concentration of alanine aminotransferase and alkaline phosphatase, with more than 75% of cats having an increase in both.
Biochemistry: hypergammaglobulinaemia; raised bilirubin without liver enzymes being raised. Hematology: lymphopenia; non-regenerative—usually mild—anaemia. Serology: the cat has a high antibody titre to FCoV: this parameter should be used with caution, because of the high prevalence of FCoV in breeding and rescue catteries.
The proportion of AST to ALT in hepatocytes is about 2.5:1, but because AST is removed from serum by the liver sinusoidal cells twice as quickly (serum half-life t 1/2 = 18 hr) compared to ALT (t 1/2 = 36 hr), so the resulting serum levels of AST and ALT are about equal in healthy individuals, resulting in a normal AST/ALT ratio around 1.
Carnitine palmitoyltransferase I (CPT1) also known as carnitine acyltransferase I, CPTI, CAT1, CoA:carnitine acyl transferase (CCAT), or palmitoylCoA transferase I, is a mitochondrial enzyme responsible for the formation of acyl carnitines by catalyzing the transfer of the acyl group of a long-chain fatty acyl-CoA from coenzyme A to l-carnitine.
All forms of portosystemic shunts produce various neurological, gastrointestinal, and urinary symptoms. [3]Symptoms of congenital PSS usually appear by six months of age [4] and include failure to gain weight, vomiting, and signs of hepatic encephalopathy (a condition where toxins normally removed by the liver accumulate in the blood and impair the function of brain cells) such as seizures ...
Famously, UGT enzymes are not present in the genus Felis, [4] and this accounts for a number of unusual toxicities in the cat family. The glucuronidation reaction consists of the transfer of the glucuronosyl group from uridine 5'-diphospho-glucuronic acid (UDPGA) to substrate molecules that contain oxygen, nitrogen, sulfur or carboxyl ...
Maropitant undergoes 1st-pass metabolism by liver enzymes, mainly CYP2D15 (which has high affinity for maropitant and clears over 90% of it) but also by the lower-affinity CYP3A12. [ 11 ] [ 12 ] Repeat dosing of maropitant eventually saturates CYP2D15, causing the drug to accumulate due to reduced clearance. [ 5 ]