Fatty acids in the remnant chylomicrons and those endogenously mobilized from adipocytes are removed by the liver, resynthesized
into triglycerides, and packaged into VLDL particles.3,7 Adipocytes mobilize fatty acids for release into the plasma by activating intracellular hormone-sensitive lipase.3,7 Hormones that stimulate this lipase include epinephrine, norepinephrine, ACTH, corticosteroids, growth hormone, and thyroid
hormone.3 An increased ratio of glucagon-to-insulin activity also stimulates fatty acid mobilization.3 VLDLs are important triglyceride transporters during fasting.7 In plasma, endothelial lipoprotein lipase splits the VLDL molecules into free fatty acids plus glycerol.3,4,7 The fatty acids of the VLDLs are removed via lipoprotein lipase.7 As the VLDLs lose fatty acids, their density increases and VLDLs become LDLs.7
LDL is VLDL minus triglyceride. LDLs are rich in cholesterol and phospholipids, and their major function is to transport cholesterol
to tissues.4,7 Cholesterol is an important component of cell membranes and hormone synthesis.4,7 Excess LDLs eventually bind to LDL receptors on hepatocytes and are removed from the plasma.7
HDL is the smallest and highest density lipoprotein.4 It is synthesized and secreted from both the liver and intestine.7 HDL comprises most of the cholesterol in dogs and cats. It serves as a reverse cholesterol transporter and scavenges excess
cholesterol from cells, returning it to the liver for excretion into the bile.4 Increased risk of cardiovascular disease is associated with increased LDL and insufficient HDL concentrations in people.
In people, LDL is considered the bad cholesterol, and HDL is considered the good cholesterol.7
Pathophysiology
Table 2: Common Causes of Hyperlipidemia in Dogs and Cats*
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Hyperlipidemia can result from dietary intake of lipids (postprandial), excessive endogenous production or mobilization of
lipids, or ineffective clearance of lipids from the serum (Table 2).3 In cases of idiopathic hyperlipidemia, the cause is not identified; however, the mechanism will be either excessive production
or mobilization or ineffective clearance.
ESSENTIAL ELEMENT
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The dietary intake of lipids is a common cause of hyperlipidemia. Hyperlipidemia can be a physiological finding in blood samples
from non-fasted animals.3 Dietary hyperlipidemia is characterized by increased chylomicron concentrations. Because chylomicrons contain mostly triglycerides
and only a small amount of cholesterol, the serum cholesterol concentration of patients with postprandial hyperlipidemia is
usually normal or only mildly increased (< 500 mg/dl). Within 30 minutes to two hours after a fat-containing meal is ingested,
chylomicrons are apparent in the plasma as a transient increase in plasma or serum turbidity.3,4 The turbidity should clear six to 10 hours after a meal.3 To avoid confusion caused by postprandial lipidemia, we recommend a 12-hour fast when evaluating blood lipid concentrations.
Endogenous mobilization of lipids results from increased intracellular hormone-sensitive lipase activity.7 Hormone-sensitive lipase activity is increased with poor nutrition (starvation, nephrotic syndrome); increased concentrations
of ACTH and corticosteroid (hyperadrenocorticism, exogenous corticosteroid administration), growth hormone (acromegaly), and
thyroid hormone (hyperthyroidism); and increased glucagon-to-insulin activity (diabetes mellitus, pancreatitis).1,3 Although hyperthyroidism increases the VLDL concentration, the concomitant increased lipoprotein lipase activity minimizes
hyperlipidemia.4 Lipoprotein lipase facilitates the movement of fatty acids from the VLDLs into cells, leaving increased serum LDL concentrations.7 Thus, hyperthyroid patients may have mildly to moderately increased serum cholesterol concentrations because of increased
LDL concentrations.1
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