The time course of metabolic changes induced by dietary cholesterol in guinea pigs

Ostwald, Rosemarie; Yamanaka, William K.; Light, Merle R.; Kroes, J.G.

doi:10.1016/0021-9150(77)90138-1

Cited by 12 publications

(5 citation statements)

References 24 publications

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“…We have previously reported a doubling of the cholesterol content of erythrocytes in cholesterol-fed anemic guinea pigs (1,2). In the present study, red cell cholesterol was shown to increase within 1-3 days after supplementation of the diet with 1 % cholesterol simultaneously with the increase of plasma cholesterol content.…”

mentioning

confidence: 44%

Spiculated Erythrocytes of Cholesterol-Fed Guinea Pigs: Changes of Morphology, Composition, and Osmotic Fragility

Aswad¹,

Ostwald²

1976

Experimental Biology and Medicine

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mentioning

confidence: 44%

Spiculated Erythrocytes of Cholesterol-Fed Guinea Pigs: Changes of Morphology, Composition, and Osmotic Fragility

Aswad¹,

Ostwald²

1976

Experimental Biology and Medicine

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“…As previous studies have shown (4,5,10,16), the liver, spleen and adrenals are organs which accumulate the greatest amount of cholesterol when the diet is enriched with this sterol, and cholesteryl ester is the predominant state of the cholesterol deposited in these organs (3,4,7,10,16). Our study shows that the amount of cholesterol deposited tends to increase with the percentage of esterified cholesterol in the same organs, except for the liver and the adrenals which seem to accumulate more cholesterol than would be predicted by the degree of esterification.…”

Section: Discussionmentioning

confidence: 88%

“…Feeding of cholesterol to animals results in metabolic alterations which vary from one animal species to another. Cholesterol-fed guinea pigs develop hypercholesterolemia with serum lipoprotein alterations (1,2), fatty liver (3) and hemolytic anemia (4)(5)(6)(7). In cholesterolfed guinea pigs as in other animal species, several mechanisms have been shown to be operating in processing the cholesterol load supplied by a diet enriched with cholesterol, such as increased excretion of bile acids (8) and decreased cholesterol synthesis (9).…”

Section: Introductionmentioning

confidence: 99%

Cholesterol esterifying capacity of various organs in cholesterol‐fed guinea pigs

Heller

1983

Lipids

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In guinea pigs fed a diet enriched with 1% cholesterol, the liver, adrenals, spleen, and small intestine accumulated cholesterol much more than the lungs and kidneys. The cholesterol content of the aorta, stomach and colon was not increased by the diet. Cholesteryl ester was the predominant form of cholesterol deposited in the organs richest in this sterol and the total cholesterol content of a tissue tended to increase with the proportion of cholesteryl ester. Cholesterol esterifying activity (ACAT) was found in most tissues and paralleled the cholesteryl ester content of these tissues, being highest in the adrenals, liver, spleen and the proximal part of the small intestine. ACAT activity was enhanced by the cholesterol diet and its elevation was fairly well correlated with the increase in the cholesterol content of the organs. However, the liver and adrenals tended to accumulate more cholesterol than anticipated from their cholesteryl ester content and their ACAT activity. Cholesterol esterification may play a major role in the ability of organs to accumulate cholesterol.

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“…Dietary cholesterol as a component of high fat diets has been shown to trigger NASH development in other animal species as well. Liver damage was also observed in guinea pigs 29,30 fed a high fat diet rich in cholesterol. In rats 31 advanced stages of NASH with severe fibrosis were only induced by high fat diets containing cholesterol but not by low cholesterol diets of otherwise identical composition.…”

Section: Evidence For the Impact Of Dietary Cholesterol On Nash Develmentioning

confidence: 91%

Dietary cholesterol does not break your heart but kills your liver

Püschel¹,

Henkel²

2018

Porto Biomedical Journal

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It is increasingly accepted that dietary cholesterol has a much lower impact on the progression of cardiovascular disease than previously assumed. However, both animal experiments and human studies seem to support the view that dietary cholesterol may contribute to the transition from benign steatosis to the potentially fatal non-alcoholic steatohepatitis. Cholesterol esters and cholesterol accumulate in the hepatocyte and impair its function. This leads to oxidative stress and endoplasmic reticulum stress triggering the release of pro-inflammatory cytokines and rendering the hepatocyte more susceptible to apoptotic or necrotic cell death. Kupffer cells group around dying hepatocytes and phagocytose the hepatocyte debris and lipids. In addition, they are exposed to lipid peroxidation products released from hepatocytes. Kupffer cells, thus activated, release pro-inflammatory, chemotactic and profibrotic cytokines that promote inflammation and fibrosis. Therefore, dietary cholesterol may be harmful to the liver, in particular when administered in combination with polyunsaturated fatty acids that favor lipid peroxidation.

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The time course of metabolic changes induced by dietary cholesterol in guinea pigs

Cited by 12 publications

References 24 publications

Spiculated Erythrocytes of Cholesterol-Fed Guinea Pigs: Changes of Morphology, Composition, and Osmotic Fragility

Spiculated Erythrocytes of Cholesterol-Fed Guinea Pigs: Changes of Morphology, Composition, and Osmotic Fragility

Cholesterol esterifying capacity of various organs in cholesterol‐fed guinea pigs

Dietary cholesterol does not break your heart but kills your liver

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