Hepatic Lipidosis in Toy Breed Dogs
Hepatic lipidosis, or fatty liver, is the condition of triglyceride accumulation in the liver which can be either physiologic or pathologic. Hepatic lipidosis can occur due to alterations in any point of normal lipid metabolism, including increased delivery of fatty acids to the liver, decreased use or oxidation of fatty acids, preferential esterification of triglycerides, choline or methionine deficiency resulting in decreased phospho-lipid synthesis, or decreased lipoprotein secretion.
In domestic animals, hepatic lipidosis most commonly occurs in cats, cows, and horses, and is usually associated with fasting or anorexia. However,increased energy demand, especially during pregnancy or lactation, diabetes mellitus, nutritional deficiencies such as choline deficiency, or hepatocellular injury can also result in hepatic lipidosis.
In dogs, hepatic lipidosis primarily occurs in young, toy-breed dogs, with Yorkshire terriers, Chihuahuas, and Fox terriers appearing to be the most susceptible. Hepatic lipidosis in young dogs is often preceded by a period of anorexia with subsequent development of hypoglycemia. Periods of anorexia are usually associated with incidences of stress, such as transfer of ownership, vaccination, weaning, tattooing, orsurgery. Young, especially toy breed, dogs are at increased risk of developing hypoglycemia because their disproportionately small muscle mass and limited hepatic glyconeogenesis capacity cannot sustain their high basal metabolic energy requirements. Large breed pups and adult dogs appear to be inherently more resistant to fasting hypoglycemia. Since adults have more developed glycohomeostatic mechanisms, they maintain normal glucagon levels, and only experience mild decreases in insulin initially which will rise slightly with prolonged fasting. In one retrospective study, the majority of pups with hepatic lipidosis presented with neurologic signs, including muscle weakness, ataxia, somnolence, convulsions, opisthotonus, and coma. These neurologic signs were attributed to cerebral neuronal necrosis due tohypoglycemia. Neurologic signs were often preceded by vomiting and diarrhea. Additionally, 40% of dogs with hepatic lipidosis had lymphoid depletion and thymic atrophy.
In experimentally fasted Yorkshire terrier pups,inadequate glyconeogenesis and hypoglycemia resulted in hypoinsulinemia, hyperglucagonemia, and ketogenesis with blood glucose levels rapidly declining when dogs were fasted more than 16 hours. Interestingly, within only eight hours of fasting, blood glucose rose above the normal values for an adult (3.9—5.0 mM/l) to more than 7.0mM/l before falling drastically below 1.0 mM/l with continued fasting. Additionally, ketone body production coincided with decreasing glucose levels.
On gross examination, puppies with hepatic lipidosis have moderately enlarged, diffusely pale yellow liver. In some cases, livers will float in formalin. Histologically, hepatocytes have diffuse microvesicular vacuolation. In a retrospective study, liver fat content with hepatic lipidosis ranged from 32-54% dry weight, as compared to a control pup that had 2% dry weight fat content.
Like cats with hepatic lipidosis, it may be beneficial to feed toy breed pups and bitches a protein-rich diet, frequently to prevent fatty liver from occurring. Such a diet may also aid in recovery from an episode ofanorexia-induced hepatic lipidosis.
-by Lisa Bartner, Michigan State University SVM Extern
-edited by Dr. Joshua Webster, ADDL Graduate Student
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