Effects of Long-Continued Cholesterol Feeding in Rats

Sperry, Warren M.; Stoyanoff, V.A.

doi:10.1093/jn/9.2.131

Cited by 23 publications

(5 citation statements)

References 18 publications

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“…Despite the large amount of cholesterol in the diet, only lipomatous lesions were observed in the coronary arteries of these rats. This result agrees with the long known fact that rats are resistant to the induction of atheromatous lesions with cholesterol feeding, alone (1,(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23), apparently because they metabolize exogenous cholesterol very efficiently. More drastic measures such as were applied in groups 5 to 9 are necessary to elevate the blood cholesterol levels of rats to such a degree that atheromatous lesions develop.…”

Section: Resultssupporting

confidence: 90%

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Experimental Atherosclerosis and Cardiac Infarcts in Rats

Wilgram

1959

The Journal of Experimental Medicine

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Atherosclerosis has been induced experimentally in several species (1, 2). However, only a few investigators have reported that life-threatening sequelae of atherosclerosis, e.g. cardiac infarcts, have been reproduced experimentally in some individual laboratory animals (3-7). We do not know why experimental atherosclerosis in laboratory animals has been so rarely accompanied by severe consequences, but many laboratories are now investigating possible differences in the clotting mechanism and other factors as causal. To aid in understanding this discrepancy between the high incidence of cardiac infarcts in man and the low incidence in laboratory animals, we developed a method by which atherosclerosis and its sequelae could be produced in rats. The rat was believed to be resistant to the induction of atherosclerosis (1, 7-22), but recently these older concepts have been revised (23-27). The rat can be induced to reproduce the equivalents of almost all the major arteriopathies that occur in man (28). I t does not respond to atherogenic regimes so readily as do the rabbit or the chicken, which is an advantage in that a more clear cut elaboration of the etiological factors is possible. This report is a confirmation and extensive enlargement of a preliminary publication in which the methods for the production of cardiac infarcts in rats have been described in detail (4, 5). Materials and MethodsA total of 135 male Wistar rats (80 gm. initial weight) was employed in this long term study. With the exception of group 1, which was fed Purina fox chow, all groups were fed the basal diet WGF-1 before they were transferred to their new diets at a weight specifically

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Section: Resultssupporting

confidence: 90%

“…Apparently this species is well equipped to dispose of a high dietary cholesterol load. This agrees with established views (1,(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23). The basal diet used in this study led to voluntary overeating and marked obesity.…”

Section: Discussionsupporting

confidence: 91%

Experimental Atherosclerosis and Cardiac Infarcts in Rats

Wilgram

1959

The Journal of Experimental Medicine

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“…Many attempts to produce this disease experimentally, based for the most part on cholesterol feeding with or without supplemental procedures, have resulted in no discernible vascular changes (3)(4)(5)(6)(7)(8)(9)(10)(11)(12). Several investigators, however, have produced lesions consisting solely of lipide infiltration of various layers of the arterial wall without other histologic changes (13,14).…”

Section: (From the Department Of Nutrition Harvard School Of Public mentioning

confidence: 99%

Experimental Production of Gross Atherosclerosis in the Rat

Fillios

Andrus

Mann

et al. 1956

The Journal of Experimental Medicine

163

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Gross atherosclerosis was produced in the rat by feeding purified diets containing cholesterol, sodium cholate, and thiouracil for periods up to 363 days. In a few weeks a marked increase of the serum cholesterol and beta lipoproteins as well as of the liver lipides was observed. Lesions visible in the gross were found on the intimal surfaces of the vessels of all 46 animals examined. These were most prominent in the heart valves and aortic arch. The earliest lesions, which were seen at 31 days, required Sudan staining for gross demonstration. Older lesions were visible without staining. Microscopic coronary artery lesions were present and in one instance were accompanied by massive myocardial infarction. Vascular lesions were characterized by medial and intimal lipide infiltration and cellular intimal plaque formation. In a part of this study the protein level of the diet was altered at the expense of sucrose. The hypercholesteremic response among the rats varied according to the dietary protein level. The lowest response was observed among those animals receiving the highest level of dietary protein. A difference, however, in the severity and extent of the arterial lesions among these relatively small groups of rats could not be established under these experimental conditions. In all these experiments a close correlation existed between the serum cholesterol levels and beta lipoproteins of the Sf20–100 range.

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“…Formation of Cholesta-3:5-dien-7-one in Rats BY N. L. KANTIENGAR* AND R. A. MORTON Department of Biochemitry, University of Liverpool (Received 18 February 1954) Addition of cholesterol to the diet of rats is well known to result in fatty infiltration of the liver (Chanutin & Ludewig, 1933;Sperry & Stoyanoff, 1934), but the process is not fully understood.…”

mentioning

confidence: 99%