Chronic Fasting Hyperlipidemia in a Cheetah (Acinonyx jubatus) and Normal Fasting Lipoprotein Levels for the Species
American Association of Zoo Veterinarians Conference 1997
Kay A. Backues1, DVM; John P. Hoover2, MS, DVM, DABVP, DACVIM; Gregory A. Campbell2, DVM, PhD, DACVP; John E. Bauer3, DVM, PhD, DACVNA; Michael T. Barrie4, DVM
1Audubon Park Zoological Park, New Orleans, LA, USA; 2Department of Medicine and Surgery (Hoover), Department of Pathology (Campbell), College of Veterinary Medicine, Oklahoma State University, Stillwater, OK, USA; 3Comparative Nutrition Research Laboratory, College of Veterinary Medicine, Texas A&M University, College Station, TX, USA; 4Oklahoma City Zoological Park, Oklahoma City, OK, USA


A severe fasting hyperlipidemia was identified in an 11-year-old male cheetah immobilized for a two-day history of vomiting, lethargy, and partial anorexia. Compensated chronic renal insufficiency, severe gastric gland atrophy, mild venous occlusive disease, and a parathyroid adenoma were also found in this animal. The hyperlipidemia was characterized by hypertriglyceridemia and hypercholesterolemia. Metabolic causes of hyperlipidemia such as chronic renal insufficiency may have contributed to the condition of this cheetah. The hyperlipidemia spontaneously resolved, but a project was undertaken to document lipoprotein normal values for the species.


Lipoproteins consist of triglycerides, cholesterol, and proteins in varying quantities which are divided into four types based on density and electrophoretic mobility. Chylomicrons and very low-density lipoproteins (VLDLs) are primarily triglyceride, the former being dietary in origin and the latter being synthesized by the liver. Low density lipoproteins (LDLs) and high-density lipoproteins (HDLs) transport cholesterol to and from the liver and body tissues.9

Hyperlipidemia refers to an increased concentration of serum lipids. Primary hyperlipidemias result from inherited defects in lipid metabolism, and secondary hyperlipidemias are indicators of underlying metabolic diseases.9,10

Diagnostic approach should first distinguish primary from secondary hyperlipidemias. Primary hyperlipidemias are uncommon and usually recognized in young animals. Depending on the enzyme defect involved, they can have severe elevations in one or more lipoproteins.5 The more common secondary hyperlipidemias cause varying hyperlipidemias. Secondary hyperlipidemias have been associated with diabetes mellitus, nephrotic syndrome, pancreatitis, hypothyroidism, chronic renal failure, and hyperadrenocorticism in animals and man.2,7,10 The type of lipoprotein that is elevated can assist in identifying a metabolic etiology.

Case Report

An 11-year-old male cheetah was examined for vomiting, lethargy, and anorexia of 2 days duration. Significant findings were moderate dehydration and a severe hyperlipidemia noted during blood sample collection after a 36-hour fast. Laboratory findings showed the cheetah to be azotemic, with blood urea nitrogen (BUN) of 69 mg/dL and creatinine of 4.0 mg/dL (International Species Information System [ISIS] reference ranges: 27–47 mg/dL and 1.6–3.2 mg/dL, respectively). A mature neutrophilic leukocytosis was present. The cheetah was treated daily with Penicillin G Benzathine and Penicillin G Procaine (Duo-Pen, G.C. Hamford MFG. Co., Syracuse, NY, USA) at 20,000 IU/kg IM, and immobilized every other day for intravenous and subcutaneous fluids for 2 weeks. Initial clinical impressions of the animal suggested pancreatitis with prerenal azotemia, though a urine sample could not be obtained to rule out renal insufficiency. Pancreatitis could not be verified due to the lack of elevated pancreatic enzymes on serum biochemical analysis. The cheetah responded to therapy with a return to normal attitude and appetite.

Persistent azotemia, submaximal urine concentration, and hyperlipidemia were found during weekly immobilizations. Chronic renal insufficiency with an idiopathic hyperlipidemia was considered at this time. Over the next 12 weeks, the animal had three episodes of mild lethargy and partial anorexia. Immobilizations were performed every 1–2 weeks for fluid administration and additional testing to find the cause of the persistent hyperlipidemia.

Other problems identified in this cheetah by biopsy were mild hepatic venous occlusive disease, moderate renal interstial fibrosis with tubular atrophy, and severe gastric gland atrophy consistent with the chronic gastritis seen in this species. The hyperlipidemia was characterized to be chylomicron in nature by the “refrigerator test.”7 To subjectively test lipoprotein lipase (LPL) activity, the animal was given intravenous sodium heparin 10,000 IU/ml (Heparin, Elkins-Sinn, Inc., Cherry Hill, NJ, USA) at 80 IU/kg. Post-heparin injection samples were less opaque than the pre-injection sample. Serum samples from the cheetah were submitted for lipid gel electrophoresis (Comparative Nutrition Research Laboratory, College of Veterinary Medicine, Texas A&M University, College Station, TX, USA) to identify the different lipoprotein particles. The electrophoresis confirmed the less sophisticated test results of a hypertriglyceridemia that was primarily chylomicron and VLDL in nature (Table 1).

Table 1. Serum triglyceride and cholesterol concentrations, and percent distribution of lipoproteins in a hyperlipidemic cheetah (Acinonyx jubatus), as determined by agarose gel electrophoresis

Lipoprotein fractions (%)

Affected cheetaha

Normal cheetahs3













Triglyceride (mg/dL)



Cholesterol (mg/dL)



aValue for affected cheetah is the average of two samples.

Twenty-four weeks after initial presentation, the fasting hyperlipidemia spontaneously resolved. Compensated chronic renal insufficiency with azotemia, isosthenuria, polydipsia, and polyuria remained. Forty-four weeks after the initial illness, the cheetah was euthanatized for uncompensated renal failure that failed to respond to aggressive fluid therapy. Hyperlipidemia was not present at euthanasia.

Significant necropsy and histology findings confirmed mild hepatic venous occlusive disease, severe chronic gastritis, and chronic renal failure with interstitial nephritis, multifocal renal fibrosis, and amyloidosis. Acute renal papillary necrosis was also present. The right parathyroid gland was markedly enlarged and histologically contained an adenoma. The pancreas was small and fibrous with no histological evidence of inflammation.


A clinical finding of hyperlipidemia is not uncommon in veterinary medicine, with postprandial hyperlipidemia being the most frequent cause.7,10 Most common metabolic etiologies such as diabetes mellitus, hypothyroidism, hyperadrenocorticism, and nephrotic syndrome were ruled out either due to lack of clinical laboratory evidence or inappropriate lipoprotein elevation.2,7,10 The exact cause of the persistent severe hyperlipidemia was not determined. Chronic renal failure was a significant finding in this cheetah and could have contributed to hyperlipidemia. In laboratory animals, experimentally-induced renal failure interfered with VLDL removal from the circulation causing hyperlipidemia that was triglyceride in nature.6 A similar pathogenesis has been suggested for the hyperlipidemia of renal failure seen in man.8 Increased parathyroid hormone can contribute to hyperlipidemia of renal failure by suppression of LPL.1 Unfortunately, it was not known whether the parathyroid adenoma in this cheetah was an active neoplasia. Pancreatitis could also have contributed to hyperlipidemia in this animal.


The authors thank Patricia Hawkins, CVT; Angie Burris, CVT; Tammy Mottl, CVT; and the Oklahoma City Zoo, Milwaukee County Zoo, and White Oak Plantation for their assistance and support of this project.

Literature Cited

1.  Akmal M, Kasim SE, Soliman AR, Massry SG. Excess parathyroid hormone adversely affects lipid metabolism in chronic renal failure. Kidney Int. 1990;37:854–858.

2.  Appel GB, Blum CB, Chien S, Kunis CL, Appel AS. The hyperlipidemia of the nephrotic syndrome. Relation to plasma albumin concentration, oncotic pressure, and viscosity. N Engl J Med. 1985;312(24):1544–1548.

3.  Backues KA, Hoover JP, Bauer JE, Barrie MT, McCann J, et al. Serum lipoproteins, thyroid hormones and resting cortisol in normal cheetahs (Acinonyx jubatus). J Zoo Wildl Med. 1997;28(4):404–406.

4.  Backues KA, Hoover JP, Bauer JE, Campbell GA, Barrie MT. Hyperlipidemia in four related male cheetahs (Acinonyx jubatus). J Zoo Wildl Med. 1997;28(4):476–480.

5.  Bauer JE, Verlander JW. Congenital lipoprotein lipase deficiency in hyperlipemic kitten siblings. Vet Clin Path. 1984;13:7–11.

6.  Gregg RC, Diamond A, Mondon CE, Reaven GM. The effects of chronic uremia and dexamethasone on triglyceride kinetics in the rat. Metabolism. 1977;26:875–882.

7.  Jones B. Feline hyperlipidemia. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. Philadelphia, PA: W.B. Saunders Co.; 1995:1410–1419.

8.  Nitzan M. Uremic hypertriglyceridemia-impaired removal versus increased production. Nutr Rev. 1977;35:95–96.13.

9.  Schaefer EJ, Levy RL. Pathogenesis and management of lipoprotein disorders. N Engl J Med. 1985;312:1300–1310.

10.  Zerbe CA. Canine hyperlipemias. In: Kirk RW, ed. Current Veterinary Therapy IX. Philadelphia, PA: W.B. Saunders Co.; 1986:1045–53.


Speaker Information
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Kay A. Backues, DVM
Audubon Park Zoological Gardens
New Orleans, LA, USA

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