Hyperlipidaemia in Dogs and Cats
World Small Animal Veterinary Association World Congress Proceedings, 2003
Faculty of Veterinary Medicine, University College Dublin, Belfield
Dublin, Ireland

Lipaemia, hyperlipaemia and hyperlipoproteinaemia all refer to increased serum lipids, usually triglyceride (TG) and/or cholesterol (CHL). CHL and TG are insoluble in water and are transported throughout the body as lipoprotein complexes. These complexes are differentiated into four main classes which can be separated by ultracentrifugation. The classes differ in lipids and apolipoprotein content and thus in size, density and electrophoretic mobility (table 1). They are chylomicron (CM), very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL).

The properties of the different lipoprotein classes in dogs and cats are similar to those in humans, but the distribution of lipid and apolipoproteins (A, B, C, E) is different. HDL is the predominant cholesterol carrier in the dog and cat.


Each class of lipoprotein has a different composition and role in lipid metabolism. The CM and VLDL are involved predominantly in TG metabolism whereas LDL and HDL are involved with CHL metabolism. As TG and/or CHL are supplied to or removed from tissues apoproteins are exchanged between the different lipoprotein classes. The enzymes lipoprotein lipase (LPL) and lecithin cholesterol acyltransferase (LCAT) are essential.

In dogs and cats a number of disorders of lipoprotein metabolism occur, resulting from either accelerated synthesis or retarded degradation of one or more of the lipoprotein classes. The causes of hyperlipidaemia in the dog and cat are listed in Table 1. Individual variations in plasma lipid concentrations are often explained by differences in dietary intake.


The presence of hyperlipidaemia may be of little clinical significance. However, it may be associated with a range of clinical signs:

 Abdominal signs--anorexia, vomiting, diarrhoea

 Acute necrotising pancreatitis--anorexia, vomiting, diarrhoea, localised abdominal pain

 Ocular abnormalities--lipid keratopathy, arcus lipoids corneae, stromal dystrophy, lipid in the aqueous humour, lipemia retinalis

 Dermatological manifestations-- cutaneous xanthomata, pruritus, Alopecia

 Central nervous system disturbances-- seizures, neuropathies, cerebral arthrosclerosis.


There are a number of useful and relatively inexpensive tests available.

1.  Measurement of serum TG and CHL. If a serum sample obtained after a 12-hour fast is lactescent it is usually caused by increased concentrations of TG (usually > 11.00mmol/L, and probably cholesterol related to elevations in CM and/or VLDL. The presence of hypercholesterolaemia in the absence of hypertriglyceridemia may not give rise to visibly lipaemic serum but it can have a hazy appearance. Normal values for TG and CHL are:

a.  Dogs: 0.56-1.7 mmol/L CHL 2.6-7 mmol/L

b.  Cats: 0.2-1.1mmol/L CHL 1-4.4 mmol/L

2.  Chylomicron test. Because of their large size and tendency to aggregate in the cold, CM rise to form a "cream" layer at the surface of a serum sample stored overnight at 4oC. If the infranatant is lactescent then this indicates VLDL elevation.

3.  Lipoprotein electrophoresis. Electrophoresis of a serum sample should reveal the four major lipoprotein bands. This test does not give quantitative results but it does indicate shifts in lipid distribution and adds support to a diagnosis.

4.  Lipoprotein separation/precipitation. Human feline electrophonetic terminology have close coincidence. These techniques provide a quantitative method of measurement and the CHL, TG and apolipoprotein concentrations can be measured within each of the lipoprotein classes. Precipitation techniques used for human lipoprotein fractionation may not accurately quantify canine and feline LDL and HDL.

5.  Lipoprotein lipase activity. The activity of LPL can be assessed by the administration of heparin which releases LPL from the capillary endothelium resulting in hydrolysis of the TG of CM and VLDL and clearing of lipemic plasma. 40 iu of heparin are administered intravenously with serum being collected before and 10 minutes after administration. If there is no change in lipid concentration or the electrophoretic patterns, then defective LPL activity should be suspected.

6.  Lipoprotein lipase mass determination. Specialist lipid research laboratories may be able to determine the amount of enzyme present.

7.  Measurement of LCAT activity.

8.  Molecular analysis. Molecular PCR analysis is available for some inherited disease e.g., one of the defects for chylomicronaemia in cats.


A diagnostic investigation plan for the dog or cat with hyperlipidemia is suggested below.

 Ensure the animal has been fasted for at least 12 hours. If lipaemia persists then further investigation is warranted.

 Determine whether the animal has hyperlipidemia secondary to an underlying metabolic disorder. Physical examination can detect abnormalities associated with diseases which cause secondary hyperlipidemia. Review the patient's history. It may provide clues to underlying diseases, especially diabetes mellitus, pancreatitis or hypothyroidism. Drugs such as Progestagens (e.g., metestrol acetate) and corticosteroids affect blood lipid levels.

 Measure serum TG and CHL in a fasting sample, and examine serum after the chylomicron refrigeration test.

 Complete appropriate biochemistry and hormone assays (thyroxine) to rule out secondary causes of hyperlipidaemia. It is important to remember that hyperlipidaemia, especially the presence of excess TG concentration in the form of CM, can interfere with complete analyses by colorimetric methods. Hyperlipemia interferes with serum direct bilirubin determination, resulting in moderate elevations. It may also decrease serum CHL, chloride, amylase, and lipase measurements and directly interfere with plasma protein and haemoglobin assays. When chylomicrons are present in excess, they displace water in a defined volume of serum thereby falsely decreasing other serum components, especially electrolytes.

 If a cause for hyperlipidaemia is found lipoprotein electrophoresis and/or ultracentrifugation is unnecessary. If the disease remains undiagnosed, then a hereditary disease must be suspected and lipoprotein ultracentrifugation is indicated to define the nature of the defect, and determine the abundance of the different lipoprotein fractions and their content.

 Further details of littermates and relatives should be sought, as some may be similarly affected.

 Further more complex investigation, including measurement of LPL or LCAT activity and molecular techniques, may identify the pathophysiological and molecular basis of the defect.


Secondary Hyperlipidaemias

Most hyperlipidaemias are secondary and are as a result of a metabolic or endocrine disease (Table 2). Hyperlipidaemia is not always present in these diseases, and there can be variations in the pattern of lipid elevation, e.g., in hypothyroidism. Hypertriglyceridaemia is often secondary to decreased clearance of TG due to reduced LPL activity but there is frequently CHL elevation.

Primary Hyperlipidaemias

Miniature schnauzer hyperlipidaemia. The pathogenesis of idiopathic hyperlipoproteinaemia in this breed is not clear, but hypertriglyceridaemia is the major abnormality. Serum CHL levels are moderately increased and LPL activity impaired. The majority of affected dogs are middle aged or older. There is not sex predisposition. Clinical signs include abdominal pain, diarrhoea, seizures and behavioural abnormalities. Many schnauzers will not show clinical signs and serum lactescence is frequently an incidental finding.

Hyperchylomicronaemia in cats. - Inherited (autosomal recessive) hyperchylomicronaemia has been described in domestic cats in New Zealand. Clinical signs occurred after 6-9 months of age and included peripheral neuropathies, cutaneous xanthomas, and the formation of lipid granulomas in abdominal organs. The disease is inherited as an autosomal recessive and homozygotes were more severely affected than heterozygotes. Most affected kittens, however, failed to show any signs other than the presence of fasting hyperlipidaemia and lipaemia retinalis. Both TG and CHL were significantly elevated. Lipoprotein fractionation revealed a marked increase in /CM and a smaller increase in VLDL. LPL was present but inactive owing to defective binding sites. The molecular basis of this disease has been identified, a point mutation in the gene. Gene transport studies have been undertaken with temporarily improved TG metabolism.

Idiopathic hyperlipidaemia. - Fasting hyperlipidaemia (chylomicronaemia) has been detected in pure-bred and mixed breed dogs and cats without a specific defect of lipid metabolism being identified. There is undoubtedly a defect in lipid metabolism; enzyme activity or receptor function which may be altered by changes in hormonal status and/or dietary challenge.

Acid cholesteryl ester hydrolase deficiency. - Described as a familial disease in young male fox terriers and characterised by hepatosplenomegaly, corneal deposits and the accumulation of cholesterol esters in the liver but serum values of CHL and TG were normal.


 The goal is to reduce plasma lipid concentrations to a value at which the risk of hyperlipidemia-associated signs is minimised (plasma triglyceride value > 5.5 mmol/L).

 Cases of secondary hyperlipidaemia are effectively treated by appropriate treatment of the underlying condition.

 Idiopathic hyperlipidaemia should be treated by dietary fat restriction. Animals that are overweight should be on calorie restriction and the owners counseled on the positive health benefits of exercise for their pet.

Failure to normalise plasma lipid concentrations may result from:

 Poor compliance with the diet.

 Ineffectiveness of the diet, which usually arises because the metabolic defect in lipoprotein metabolism can not be entirely corrected by a reduced fat intake.

 Failure to lose weight if obese.

 Development of secondary hyperlipidaemia in cases where underlying disease was not obvious on initial investigation. In such cases, the animal should be re-evaluated.


Dietary changes are designed to reduce the intake of fat, mainly triglycerides, and thus reduce the production of chylomicrons and VLDL. Ideal characteristics of a lipid-reducing diet include:

 Low fat content; low in saturated fats and high in polyunsaturated fatty acids. Omega-3 (n-3) fatty acids have specific hypotriglyceridemic effects that are not simply the result of displacement of saturated fat from the diet.

 High fibre content; water-soluble fibre limits fat absorption and enhances biliary excretion of cholesterol.

 Moderate carbohydrate content. Diets excessively high in carbohydrates will increase plasma triglyceride concentrations by supplying excess lipogenic substrates.

Commercial veterinary diets are available which fulfill these criteria.


Most human drugs are not licensed for use in dogs and cats. Certain agents have, however, been used in dogs and cats and there are anecdotal reports of successful treatment. These drugs are to be used with caution and every effort made to monitor the health status and blood biochemistry and haematology of any animals on treatment.

1.  Bile acid sequestrants: These bind bile acids in the intestinal tract and limit their enterohepatic circulation, thereby reducing the supply of cholesterol to the liver. This results in up-regulation of hepatic LDL-receptor activity and consequent lowering of plasma LDL and cholesterol concentrations.

2.  HMG CoA-reductase inhibitors: commonly referred to as 'statins', these drugs reduce hepatic cholesterol synthesis and so up-regulate LDL-receptor activity. There are the most powerful cholesterol-lowering agents available, and much of their toxicological testing was performed in dogs where a good safety profile was demonstrated.

3.  Marine (fish) oils: These oils are rich in n-3 fatty acids and appear to reduce plasma triglyceride concentrations by decreasing the synthesis of VLDL. 10-30 mg/kg PO every 24 hours as the first line of drug therapy in dogs with hypertriglyceridaemia that is unresponsive to dietary fat restriction alone has been used successfully.,

4.  Nicotinic acid and fibric acid derivatives: These act primarily to reduce hepatic triglyceride synthesis and are most commonly used in the management of moderate hypertriglyceridemia. Certain of the new agents, e.g., acipimox, also act to reduce adipose lipolysis. I have used gemfibrozil (Lopid, Parke Davis) in dogs and cats with hypertriglyceridaemia that has not been controlled by a low fat diet alone and noted no untoward side-effects at does of 150-300mg PO every 12 hours for dogs and 7.5-10 mg/kg for cats.

Table 1: Physical Characteristics of Canine and Feline Lipoproteins (after Bauer, 2000)

Lipoprotein/ Function

Size (nm)

Hydrated Density (g/ml)

Mobility (ElectropPhoresis)

Major Apo-Proteins

Chylomicrons-dietary lipid transport

Dog, cat





VLDL-hepatic TG/cholesterol transport

Dog, cat




B100, B48, E, C

LDL-cholesterol transport





B100, B48






HDL1(HDLc)- reverse cholesterol transport





E, A, C

HDL2-reverse cholesterol transport





E, A, C





E, A-I, C

HDL3-reverse cholesterol transport

Dog, Cat




A, C

VLDL = very low-density lipoprotein; TG = triglyceride, LDL = Low-density lipoprotein; HDL = high-density lipoprotein

Table 2: Causes of Hyperlipidaemia in the Dog and Cat

Post Prandial Hyperlipidaemia







--Diabetes mellitus



--Liver disease






--Nephrotic syndrome













--Idiopathic hyperlipidemia of miniature schnauzers



--Idiopathic hyperlipidemia, other



--Hyperchylomicronaemia of cats



--Acid Cholesteryl ester hydrolase deficiency




References are available upon request.

Speaker Information
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Faculty of Veterinary Medicine, University College Dublin, Belfield
Dublin, Ireland

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