The Effects of Feeding Various Dietary Fats on the Development and Regression of Hypercholesterolemia and Atherosclerosis

Vesselinovitch, Dragoslava

doi:10.1007/978-1-4615-9029-3_5

Cited by 23 publications

(6 citation statements)

References 17 publications

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“…Butter and other dairy fats (high in 14 : 0, myristic acid) most strongly increase LDL, beef fat (containing palmitic acid, 16 : 0; stearic acid, 18 : 00) raised LDL to a lesser degree and cocoa butter (containing largely stearic acid) raises LDL only slightly [12,51]. Medium-chain saturated fats, such as those found in coconut fat, appear to be more atherogenic in animals than predicted solely on the basis of their relationship with serum cholesterol [4], but they potently increase HDL cholesterol [52]. In one of the few attempts to investigate specific saturated fatty acids in prospective observational studies, Hu et al [53] found that they were strongly correlated with each other and thus their effects were difficult to separate; however, stearic acid was most strongly associated with risk of CHD.…”

Section: Further Aspects Of Dietary Fats and Chdmentioning

confidence: 93%

“…Early interest in the relation between dietary fats and cardiovascular disease emerged from animal studies conducted during the 1930s, showing that dietary cholesterol causes arterial lesions and that this is mediated largely through elevation in blood cholesterol levels [1][2][3][4][5]. Subsequent studies of heart disease rates in different populations, controlled feeding studies on the effects of dietary fats on serum cholesterol and epidemiologic studies relating serum cholesterol to risk of coronary heart disease (CHD) risk led to the conclusion that high intake of saturated fat is a major cause of heart disease.…”

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confidence: 99%

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Dietary fats and coronary heart disease

Willett

2012

Journal of Internal Medicine

244

136

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Section: Further Aspects Of Dietary Fats and Chdmentioning

confidence: 93%

mentioning

confidence: 99%

Dietary fats and coronary heart disease

Willett

2012

Journal of Internal Medicine

244

136

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“…31 The loss of macrophages, as we have observed, bears a striking resemblance to the findings in classic studies in nonhuman primates. [32][33][34] As summarized by Small, 35 when diet-sensitive monkeys, such as Macaca fascicularis, were fed a high-cholesterol diet for 18 months to induce lesions then switched to low-cholesterol feeding, serial changes in the lesions also demonstrated a loss in foam cells. These similarities indicate that the regression of atherosclerotic lesions may be achieved by processes that are common among a number of mammalian species, adding support to the relevance of our findings to humans.…”

Section: Trogan Et Al Regression Of Mouse Atherosclerosis By In Vivo Mrimentioning

confidence: 99%

Serial Studies of Mouse Atherosclerosis by In Vivo Magnetic Resonance Imaging Detect Lesion Regression After Correction of Dyslipidemia

Trogan

Fayad

Itskovich

et al. 2004

ATVB

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Objective-We determined the effects of sustained normocholesterolemia on advanced mouse atherosclerosis and whether changes in plaque size and composition can be detected noninvasively by MRI. Methods and Results-Aortic arch segments containing advanced lesions from apolipoprotein E-deficient (apoEϪ/Ϫ) mice (total cholesterol 1281Ϯ97 mg/dL) were transplanted into syngeneic wild-type (WT; 111Ϯ11 mg/dL) or apoEϪ/Ϫ (702Ϯ74 mg/dL) recipient mice on chow diet. Mice underwent serial MRI at 3, 5, 7, and 9 weeks after transplantation. Compared with 3 weeks, correction of dyslipidemia in WT recipient mice resulted in a monotonic decrease (regression) in arterial wall volume, whereas in apoEϪ/Ϫ recipient mice, further plaque progression was noted (PϽ0.05). MRI and histological measurements were closely correlated (Rϭ0.937). The lesional content of macrophages decreased Ͼ90% (PϽ0.001), and smooth muscle cells increased in the WT recipient mice. In vivo T 1 -, T 2 -, and proton density-weighted images of the mouse thoracic aorta differentiated intraplaque lipid and collagen. Conclusions-Plaque changes can be noninvasively monitored by serial in vivo MRI of a mouse regression model. Our ability to image the thoracic aorta and perform in vivo plaque characterization will further enhance atherosclerosis studies. Key Words: atherosclerosis Ⅲ imaging Ⅲ lipoproteins Ⅲ remodeling Ⅲ transplantation P laque regression in mouse models of atherosclerosis has previously been demonstrated primarily by somatic adenoviral gene transfer. 1,2 Such approaches have been limited because of the eventual loss of transgene expression, even with second-generation viral vectors, likely caused by immune responses directed against both the transgene product and adenoviral proteins. 3,4 In addition, regression has typically been inferred from ex vivo histological tissue sampling of numerous animals at multiple time intervals after treatment or perturbation. It would be of obvious advantage to be able to use in vivo MRI to noninvasively monitor, quantify, and characterize plaque in a model where the regressive conditions are constant and sustained indefinitely.Mice have become widely used as models of human atherosclerosis because they offer the advantages of ample progeny, a well-characterized genome similar to that of humans, and the relative ease of genetic manipulations. Apolipoprotein E-deficient (apoEϪ/Ϫ) mice spontaneously develop lesions which resemble those found in humans. 5,6 However, unlike in large animals, in apoEϪ/Ϫ mice neither dietary manipulation nor treatment with statins 7 corrects hyperlipidemia. Tsukamoto et al 8 used adenoviral expression of an apoE transgene in these mice to promote the clearance of the atherogenic lipoprotein particles and correct the dyslipidemia. The expression of the transgene, however, was short-lived, lasting Ϸ3 months. In a modified approach, Desurmont et al 1 used immunocompromised mice in a nude background to prolong the expression of adenoviralexpressed apoE; however, the complete lack of mature cytot...

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“…The level of cholesterol was closely related to death from both CHD and all causes [6]. In addition, because cholesterol-induced arterial lesions in animals were somewhat similar to human atherosclerosis, the pathogenic mechanism was considered to be settled [7], and the way to prevention largely opened. Unfortunately, the way to prevention has been rougher than expected.…”

Section: Introductionmentioning

confidence: 99%

Dietary fats and coronary heart disease pathogenesis

Renaud

Lanzmann‐Petithory

2002

Curr Atheroscler Rep

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The intake of saturated fat seems to be the main environmental factor for coronary heart disease (CHD). However, decreasing the intake of saturated fat and replacing it in part with linoleic acid in primary or secondary intervention trials did not satisfactorily reduce CHD clinical manifestations. It is only when omega-3 fatty acids, alpha-linolenic acid (ALA), or eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were added to the diet that sudden cardiac death (ALA, EPA plus DHA) and nonfatal myocardial infarction (only ALA) were significantly lowered. The protective effect of omega-3 fatty acids occurs rapidly, within weeks. The mechanism for preventing ventricular fibrillation seems to be through a direct effect on myocytes. The additional effect of ALA on nonfatal myocardial infarction may be through thrombosis, at least partly caused by an effect on platelets.

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The Effects of Feeding Various Dietary Fats on the Development and Regression of Hypercholesterolemia and Atherosclerosis

Cited by 23 publications

References 17 publications

Dietary fats and coronary heart disease

Dietary fats and coronary heart disease

Serial Studies of Mouse Atherosclerosis by In Vivo Magnetic Resonance Imaging Detect Lesion Regression After Correction of Dyslipidemia

Dietary fats and coronary heart disease pathogenesis

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