Hypercholesterolemia and hypertriglyceridemia as biochemical markers of disease in companion rabbits.

BACKGROUND: Inflammation has important effects on lipid metabolism, but the relationship between hyperlipidemia, inflammation, and disease remains unknown in rabbits. While rabbits are sensitive to dietary hypercholesterolemia, the etiology of hyperlipidemia when fed non-atherogenic diets is uncertain. OBJECTIVES: This study aimed to determine the association between hypercholesterolemia and patient characteristics, diseases, and select CBC and biochemistry analytes in rabbits, and to measure plasma lipoprotein lipid fractions in rabbits with inflammatory and other diseases. METHODS: Complete blood count and plasma biochemistry data, including total cholesterol concentrations, were evaluated in 531 companion rabbits. Lipoprotein cholesterol fractions (non-high-density lipoprotein cholesterol [non-HDLc] and high-density lipoprotein [HDLc]) and triglycerides were measured using a colorimetric enzymatic assay in archived plasma from a subset of 267 rabbits. Rabbits were categorized by age, sex, spay/neuter status, breed, diet status (fed atherogenic dietary components or not), the organ system affected by disease, and the pathologic process. RESULTS: Cholesterol was associated with fibrinogen (P = 0.01), globulins (P < 0.01), and heterophil (P < 0.01) concentrations. Adjusting for diet, rabbits with severe infection or sepsis (odds ratio [OR] = 13.25, 95% CI = 5.83-30.12), renal failure (OR = 14.42, 95% CI = 5.69-36.54), and hepatopathy (OR = 8.55, 95% CI = 3.55-20.62) had increased risks of hypercholesterolemia. Increased non-HDLc and triglyceride concentrations were also associated with these three disease states (P < 0.05). CONCLUSIONS: Hyperlipidemia is associated with biochemical and CBC markers of inflammation, and with severe infection or sepsis, renal failure, and hepatopathy. Independent of diet, increased cholesterol, non-HDLc, and triglycerides are indicators of disease in companion rabbits.

Modulation of lipid homeostasis in response to continuous or intermittent high-fat diet in pigs.

A high-fat diet is known to induce atherosclerosis in animal models. Dietary factors and timing of atherogenic food delivery may affect plasma lipoprotein content composition and its potential atherogenic effect. Increasingly often, humans spend periods/days eating in a completely unregulated way, ingesting excessive amounts of food rich in oils and fats, alternating with periods/days when food intake is more or less correct. We investigate the effect on lipid homeostasis of a high-fat diet administered either continuously or intermittently. We investigated control pigs receiving standard diet (C, n=7), pigs receiving a high-fat diet every day for 10 weeks (CHF, n=5), and pigs receiving a high-fat diet every other week for 10 weeks (IHF, n=7). IHF animals were shown to have a different lipid profile compared with CHF animals, with a significant increase in high-density lipoproteins (HDL) levels with respect to C and CHF groups. CHF also showed significantly higher values of TC/HDL cholesterol compared with C and IHF. Hepatic expression analysis of genes involved in lipid homeostasis showed an increasing trend of nuclear receptor LXRα along with its target genes in the CHF group and in the IHF group, whereas SREBP2 and LDLr were significantly inhibited. A significant correlation was found between ABCA1 expression and circulating levels of HDL-C. Periodic withdrawals of a high-fat atherogenic diet compared with a regular administration results in a different adaptive response of lipoprotein metabolism, which leads to a significantly higher plasma level of HDL-C and lower TC/HDL-C.

Experimental diet-induced atherosclerosis in Quaker parrots (Myiopsitta monachus).

Spontaneous atherosclerosis is common in psittaciformes, and clinical signs associated with flow-limiting stenosis are encountered in pet birds. Nevertheless, a psittacine model of atherosclerosis has not been developed for research investigations. Sixteen captive-bred Quaker parrots (Myiopsitta monachus) were used in this study. While 4 control birds were fed a maintenance diet, 12 other birds were fed an atherogenic diet composed of 1% cholesterol controlling for a calorie-to-protein ratio for periods ranging from 2 to 8 months. The birds were euthanized at the end of their respective food trial period. Histopathology, transmission electron microscopy, and cholesterol measurement were performed on the ascending aorta and brachiocephalic and pulmonary arteries. Plasma lipoproteins, cholesterol, and triglycerides were also measured on a monthly basis. Significant atherosclerotic lesions were induced within 2 months and advanced atherosclerotic lesions within 4 to 6 months. The advanced lesions were histologically similar to naturally occurring lesions identified in the same parrot species with a lipid core and a fibrous cap. Ultrastructurally, there were extracellular lipid, foam cell, and endothelial changes. Arterial cholesterol content increased linearly over time. Plasma cholesterol and low-density lipoprotein (LDL) significantly increased over time by an average of 5- and 15-fold, respectively, with a shift from high-density lipoprotein to LDL as the main plasma lipoprotein. Quaker parrots also exhibited high plasma cholesteryl ester transfer protein activity that increased, although not significantly, over time. This experiment demonstrates that in Quaker parrots fed 1% cholesterol, advanced atherosclerosis can be induced relatively quickly, and lesions resemble those found in other avian models and humans.