Atherogenesis in swine fed several types of lipid‐cholesterol diets

Goldsmith, Dale P. J.; Jacobi, Herbert P.

doi:10.1007/bf02533395

Cited by 8 publications

(3 citation statements)

References 23 publications

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“…There are qualitative differences in the atherogenicity of various dietary fats (Aguilera et al, 2002). Coconut oil is more atherogenic than other saturated, monunsaturated, and polyunsaturated fats (Goldsmith and Jacob, 1978;Kritchevsky et al, 2003;Pronczuk et al, 1991). The recognition of hyper-triglyceridemia as a synergistic and recently as an independent risk factor for cardiovascular disease (Assmann et al, 2002;Ginsberg et al, 1995;Pearson et al, 2002;Stensland-Bugge et al, 2000) suggests that dietary models of atherosclerosis should include elevation of plasma triglyceride levels.…”

Section: Diet-induced Hypercholesterolemiamentioning

confidence: 99%

Physical Activity and Atherosclerosis: Which Animal Model?

Turk¹,

Laughlin²

2004

Can. J. Appl. Physiol.

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Atherosclerosis is a progressive disease that is the most important single contributor to human cardiovascular morbidity and mortality. Epidemiologic studies show that physical activity, or routine exercise, reduces the risk of developing cardiovascular disease. The mechanisms through which exercise may function in primary or secondary prevention of atherosclerosis remain largely to be established. Most studies in humans are performed after the onset of clinical signs when disease is well advanced and the prescription of exercise is based on empirical evidence of benefit in secondary prevention. Animal models per-mit the study of the initiation and progression of preclinical stages of atherosclerosis. In order to provide information relevant to treatment and prevention, these models should mimic human disease and interactions of physical activity with disease processes as closely as possible. The purpose of this review is to compare animal models of atherosclerosis and to summarize the available data in those models in regard to the effects of exercise.

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Section: Diet-induced Hypercholesterolemiamentioning

confidence: 99%

Physical Activity and Atherosclerosis: Which Animal Model?

Turk¹,

Laughlin²

2004

Can. J. Appl. Physiol.

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“…The VLDL (d< 1.006 g/mL) cholesterol concentration in NL was 4.23, in FHC 3.37, and in DHC 45.66 mg/dL. Sera and HDL supernatant (serum after selective precipitation of apoBcontaining particles used to assay HDL-C) from all three groups showed a-migrating apoA-I, whereas FHC and DHC also showed a /3-migrating form of apoA-I that corresponds to the pre-/3-migrating lipoproteins15.5 ng of proteins, respectively; and lanes A4, B4, and C4 contain 2 fit of layer 4 (d= 1.054-1.21 g/mL) with 12.4, 25.4, and 6.8 ^g of proteins. The layers were washed at their upper densities (see "Methods").…”

mentioning

confidence: 92%

Familial and diet-induced hypercholesterolemia in swine. Lipid, ApoB, and ApoA-I concentrations and distributions in plasma and lipoprotein subfractions.

Hasler‐Rapacz

Nichols

Griggs

et al. 1994

Arterioscler Thromb

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Low levels of high-density lipoproteins (HDLs) may constitute an independent risk factor that may be as important as elevated low-density lipoproteins (LDLs) in coronary artery disease (CAD). Concentrations and distributions of lipids, apolipoprotein (apo) B, and apoA-I in the plasma and lipoprotein subfractions of two groups of swine, one with familial hypercholesterolemia (FHC) and the other with diet-induced hypercholesterolemia (DHC), were examined. Normolipidemic (NL) animals served as controls. All pigs carried the Lpb5 apoB mutation, which is known to influence the formation of atherosclerotic lesions. Mean concentrations of serum total cholesterol in NL, DHC, and FHC were 80.0+9.3, 774.3±54.5, and 316.5±36.1 mg/dL, respectively; HDL cholesterol (HDL-C), 33.5±1.9, 137.0±9.9, and 22.3±2.2 mg/dL; triglycerides, 33.0+16.3, 40.3±11.7, and 56.8±7.2 mg/dL; apoB, 35.7±3.1, 142.0±4.8, and 169.3+13.9 mg/dL; and apoA-I, 62.4±9.3, 170.9±6.9, and 42.6±4.8 mg/ dL. The distributions of total cholesterol, apoB, and apoA-I in plasma lipoprotein subfractions were also examined. Compared with NL, FHC had fourfold and 4.7-fold increases in total cholesterol and apoB, respectively, distributed in the lower densities (d< 1.043 g/mL), and low HDL-C and apoA-I levels, resulting in a high total cholesterol/HDL-C ratio (14.4:1) and elevated triglyceride levels. DHC was characterized by 10-fold and fourfold increases in total cholesterol and apoB, respectively, resulting in an LDL particle highly enriched in cholesterol, a fourfold increase of HDL-C, an almost threefold increase in apoA-I, and a normal triglyceride level. Thus FHC but not DHC exhibited a marked resemblance to familial combined hyperlipidemia, the most common endogenous dyslipidemia in humans. (Arterioscler Thromb. 1994;14: 923-930.) Key Words • swine • familial hypercholesterolemia • diet-induced hypercholesterolemia • plasma cholesterol • HDL cholesterol • apoB • apoA-I • triglycerides • immunochemistry at NORTH DAKOTA STATE UNIV on June 17, 2015 http://atvb.ahajournals.org/ Downloaded from at NORTH DAKOTA STATE UNIV on June 17, 2015 http://atvb.ahajournals.org/ Downloaded from J O Hasler-Rapacz, T C Nichols, T R Griggs, D A Bellinger and J Rapacz concentrations and distributions in plasma and lipoprotein subfractions. Familial and diet-induced hypercholesterolemia in swine. Lipid, ApoB, and ApoA-I

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“…' The current study uses a model of coronary atherosclerosis in swine to address the relationship between the degree of atherosclerosis as assessed by antemor-tem coronary angiographic examination and that seen in pathologic examination of the coronary arteries fixed by perfusion at physiologic pressure. [8][9][10][11][12][13] Methods Seven 12 to 15-week-old male Yorkshire pigs from a stable breeding stock were studied. After initial determination of plasma lipid levels, the animals were placed on a high-cholesterol, high-fat diet (table 1), which was continued for the duration of the study.…”

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confidence: 99%