The Biological Value of Oils and Fats III. The Longevity of Rats Fed Rapeseed Oil or Butterfat-Containing Diets

Thomasson, H. J.

doi:10.1093/jn/57.1.17

Cited by 25 publications

(5 citation statements)

References 11 publications

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“…It is well-known that high-erucic-acid rapeseed oil feeding develops transient cardiac lipidosis in animals as well as in humans, and the imbalance between the input and oxidation of erucic acid was proposed to be a critical cause for the acute lipid deposition in heart (1)(2)(3). High-erucic-acid rapeseed oil feeding also caused lipid deposition in liver; however, the effect of erucic acid on hepatic steatosis was progressive and irreversible (4,5); therefore, the mechanism that led to lipid deposition in liver was distinct from that in heart. As mitochondrial fatty acid oxidation plays a central role in liver fatty acid metabolism, it is rational to assume that metabolism of erucic acid might negatively regulate mitochondrial fatty acid oxidation and lead to hepatic steatosis.…”

mentioning

confidence: 97%

Peroxisomal oxidation of erucic acid suppresses mitochondrial fatty acid oxidation by stimulating malonyl-CoA formation in the rat liver

Chen

Shang

Deng

et al. 2020

Journal of Biological Chemistry

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Feeding of rapeseed (canola) oil with a high erucic acid concentration is known to cause hepatic steatosis in animals. Mitochondrial fatty acid oxidation plays a central role in liver lipid homeostasis, so it is possible that hepatic metabolism of erucic acid might decrease mitochondrial fatty acid oxidation. However, the precise mechanistic relationship between erucic acid levels and mitochondrial fatty acid oxidation is unclear. Using male Sprague–Dawley rats, along with biochemical and molecular biology approaches, we report here that peroxisomal β-oxidation of erucic acid stimulates malonyl-CoA formation in the liver and thereby suppresses mitochondrial fatty acid oxidation. Excessive hepatic uptake and peroxisomal β-oxidation of erucic acid resulted in appreciable peroxisomal release of free acetate, which was then used in the synthesis of cytosolic acetyl-CoA. Peroxisomal metabolism of erucic acid also remarkably increased the cytosolic NADH:NAD+ ratio, suppressed sirtuin 1 (SIRT1) activity, and thereby activated acetyl-CoA carboxylase, which stimulated malonyl-CoA biosynthesis from acetyl-CoA. Chronic feeding of a diet including high-erucic-acid rapeseed oil diminished mitochondrial fatty acid oxidation and caused hepatic steatosis and insulin resistance in the rats. Of note, administration of a specific peroxisomal β-oxidation inhibitor attenuated these effects. Our findings establish a cross-talk between peroxisomal and mitochondrial fatty acid oxidation. They suggest that peroxisomal oxidation of long-chain fatty acids suppresses mitochondrial fatty acid oxidation by stimulating malonyl-CoA formation, which might play a role in fatty acid–induced hepatic steatosis and related metabolic disorders.

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mentioning

confidence: 97%

Peroxisomal oxidation of erucic acid suppresses mitochondrial fatty acid oxidation by stimulating malonyl-CoA formation in the rat liver

Chen

Shang

Deng

et al. 2020

Journal of Biological Chemistry

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“…The fiber content of feeds containing high amounts of sunflower oil must also be considered. Diets rich in fiber tend to reduce the efficiency of absorption and food utilization [Morgan et al, 1974;Van halite, 1978], In addition, a high sunflower oil consumption itself might cause a growth inhibition [Thomasson, 1955]. In our experiment, the diet poor in protein and rich in oil as an imbalanced diet was especially noxious to the young rats' growth.…”

Section: Discussionmentioning

confidence: 65%

Effect of Dietary Protein and Lipid on the Activity of Hepatic Mixed-Function Oxidase System in Young and Adult Rats

1982

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Effects of marginal or normal casein diets with different sunflower oil contents were tested on the hepatic mixed-function oxidase system in young and adult male rats. The weight gain and the activity of aminopyrine demethylase, aniline hydroxylase and the content of cytochrome P-450 was decreased only in young rats fed 10% casein and 10% oil containing diets. Both in young and adult animals, independently of casein consumption, the activity of MFO with the exception of cytochrome P-450 in adult rats fed 20% casein was significantly higher when the level of dietary sunflower oil was shifted from 10 to 30%.

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“…In general, butterfat and lard increased the growth rate and decreased longevity while fats· rich in unsaturated fatty acids had the opposite effect (63,64). Those fats which increased the growth rate also increased the food intake of the rats and vice versa.…”

Section: Fats and Fatty Acidsmentioning

confidence: 94%

Nutrition and Nutritional Deficiency Diseases

Rw¹,

Jj²

1958

Annu. Rev. Med.

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The Biological Value of Oils and Fats III. The Longevity of Rats Fed Rapeseed Oil or Butterfat-Containing Diets

Cited by 25 publications

References 11 publications

Peroxisomal oxidation of erucic acid suppresses mitochondrial fatty acid oxidation by stimulating malonyl-CoA formation in the rat liver

Peroxisomal oxidation of erucic acid suppresses mitochondrial fatty acid oxidation by stimulating malonyl-CoA formation in the rat liver

Effect of Dietary Protein and Lipid on the Activity of Hepatic Mixed-Function Oxidase System in Young and Adult Rats

Nutrition and Nutritional Deficiency Diseases

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