The fed camelid supplies most of its body energy needs through the short chain fatty acid products of gastric fermentation.
These are made in roughly the same proportion as in ruminants on similar diets, with the difference that the camelid gastric
wall does not appear to convert butyrate to its ketone form. Short chain fatty acids may be oxidized by most tissues.
The feed-deprived camelid mobilizes peripheral adipose stores for energy. As far as we know, this intracellular lipolysis
occurs under similar hormonal conditions as in other species; that is, catecholamines and possibly some other hormones stimulate
lipolysis, whereas insulin inhibits it. Glucocorticoids appear to have little effect.
The free fatty acids liberated from adipose tissue circulate bound to albumin. The consequences of hypoalbuminemia, a common
finding in sick camelids, on this transport is unknown. The fatty acids are taken up be cells in proportion to their blood
concentrations, and can be oxidized by most tissues for energy. However, more metabolically active cells are unable to enhance
uptake of these substrates.
The liver plays a central role in modifying free fatty acids for use by other tissues. Several types of conversion are possible,
the most important of which are modification to water-soluble ketone bodies or reesterification to triglyceride for export
as Very Low Density Lipoproteins. Lipoproteins carry triglyceride through the bloodstream, where free fatty acid may be liberated
locally (intravascular lipolysis) by the action of lipoprotein lipase. Insulin, insulin-like growth factors, and thyroid hormone
stimulate lipoprotein lipase activity, whereas some inflammatory mediators inhibit it.
Disorders of Lipid Metabolism
Starvation/Dietary insufficiency results in mobilization of adipose stores. In general, camelids are quite resilient to pathologic effects of starvation.
Experimentally, pregnant and/or lactating camelids on restricted diets may develop rapid fat mobilization, possibly resulting
in hepatic lipidosis. Non-pregnant, non-lactating camelids develop a lower degree of fat mobilization and do not accumulate
lipid in their liver.
Natural cases demonstrate that even non-pregnant, non-lactating camelids may develop lipidosis or lipemia, but it is assumed
that some factor beyond dietary insufficiency is contributing.
Hepatic Lipidosis Although pregnant or lactating females make up the majority of camelids seen at our clinic with hepatic lipidosis, their
proportion does not differ significantly from their proportion in the overall hospital population. Most show an increase in
blood NEFA and ketones, reflective of peripheral fat mobilization and oversupply to the liver. Some also have hyperlipemia
(an increase in triglycerides and cholesterol) with concurrent hyperketonemia and hyperglycemia. Blood glucose is rarely low,
except in pregnant or lactating females, and is frequently even high. This suggests that pregnant or lactating females may
develop hepatic lipidosis when their blood glucose supply does not match demand, a similar situation to ketosis in cattle
or sheep. Non-pregnant and non-lactating camelids, which have no particularly remarkable energy demand, may have some end-utilization
In addition to simple starvation or competition for food, various stressors may promote lipolysis. These include transport,
extreme temperatures, hypoproteinemia, and illness. Concurrent or previous liver disease may compromise its function in energy
meatoblism. Hormonal mechanisms may also play a role, especially suppression of insulin production or increase in catecholamines.
Protein deficiency appears to play a greater role than in cattle. Hypoalbuminemic hypoproteinemia is common in sick camelids,
including those with lipidosis. Healthy camelids seek out high-protein plants in an environment, and appear to tolerate intermittent
starvation well. It is our belief that they tolerate caloric malnutrition (marasmus) much better than they tolerate protein-calorie
malnutrition (kwashiorkor). The reasons for this are unknown but may include the following: as in cows, vital amino acid deficiencies
may prevent lipoprotein formation and result in hepatic lipidosis; amino acid deficiencies may inhibit the production of vital
protein hormones, such as insulin; and the enzymatic pathways that direct glucose and pyruvate away from the citric acid cycle
may increase need for other components (amino acids) to enter that cycle to replenish oxaloacetate and to produce energy.
Hyperlipemia may be seen with other indicators of negative energy balance, or as the sole abnormality. With more severe hyperlipemia,
it becomes more likely that other blood fat fractions are high. As with lipidosis, all ages and signalments of camelid are
affected by hyperlipemia.(ref) Camelids appear to be either more capable than cattle of exporting liver triglyceride as lipoprotein,
or they have greater problems with end-utilization. In camelids with hepatic lipidosis, hyperlipemia appears to be a late
condition, almost terminal, and likely reflects extreme catecholamine stimulation and inhibition of intravascular lipolysis.
In other camelids, hyperlipemia appears to relate to inflammation, so prostaglandin inhibition of lipoprotein lipase must
Recent findings suggest mild hyperlipemia tends to worsen unless specifically treated, even if any underlying disorders are
appropriately addressed. Thus, even mild hyperlipemia may represent the beginning of a serious, progressive metabolic derangement.