Feline hepatic lipidosis (FHL) is the most common liver disease affecting cats. It is considered a consequence of prolonged starvation often secondary to loss of appetite due to presence of another illness. The exact mechanisms remain elusive but involves an imbalance between the mobilization of fat from peripheral fat stores into the liver and synthesis of fatty acids (FA) in the liver on the one hand, and the decreased metabolism (oxidation) of liver FA and removal of fat from the liver via very-low density lipoproteins (VLDL). Buildup of fat in the liver ensues leading to liver dysfunction.
It has been suggested that a lower capacity to excrete VLDL from the liver plays a role in the development of FHL. Secretion of VLDL is dependent on the rate of hepatic phosphatidylcholine (PC) synthesis. PC is synthetized in the liver by two pathways, the Kennedy pathway and the phosphatidylethanolamine N-methyltransferase (PEMT) pathway. Both choline deficiency and low PEMT activity are associated with hepatic lipidosis in humans, mice and rats. In these species, PEMT expression and activity is upregulated by oestrogens. Therefore, it has been postulated that spaying female cats could increase their risk for developing FHL. Indeed, one study by Center et al. (1993)1 reported that female cats are more affected than male cats; nevertheless, it is more commonly reported that FHL has no breed, age or sex predisposition.
Researchers from University of Utrecht, The Netherlands evaluated the change in liver PEMT activity and choline plasma levels in cats before and after spaying/neutering. Six intact female and six intact male client-owned cats were enrolled into the study. The cats were fed a diet with recommended dietary choline content. PEMT activity was assayed directly in liver biopsies taken before and 4 weeks after spaying/neutering, and assessed indirectly by analyses of PEMT–specific hepatic PC species and plasma choline levels. Hepatic PEMT activity did not differ between intact female and male cats and no statistical significant changes upon spaying/neutering were observed.
In conclusion, it is unlikely that castration predisposes cats for FHL by causing PC deficiency as suggested in other species when recommended dietary choline level are fed.