Induction of peroxisomal β-oxidation in rat liver by high-fat diets

Liver peroxisomes were prepared by using a Percoll gradient in a vertical rotor. beta-Oxidation was measured in peroxisomes isolated from livers of rats fed on either high-(15% by wt.) or low- (5% by wt.) fat diets. The feeding of high-fat diets gave a 1.4-2.4-fold increase in total liver peroxisomal beta-oxidation, and a similar increase in specific activity. A 1.5-4.5-fold increase was seen in the specific activity of purified peroxisomal preparations. The reasons for these increases are discussed.

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Characterization of the stimulatory effect of high-fat diets on peroxisomal β-oxidation in rat liver

Biochemical Journal ◽

10.1042/bj2060195 ◽

1982 ◽

Vol 206 (2) ◽

pp. 195-202 ◽

Cited By ~ 82

Author(s):

M S Thomassen ◽

E N Christiansen ◽

K R Norum

Keyword(s):

Fatty Acid ◽

Fold Increase ◽

Soya Bean ◽

High Fat ◽

Beta Oxidation ◽

Rape Seed ◽

Oxidation Activity ◽

Marine Oil ◽

High Fat Diets ◽

Fat Diets

1. The effect on rat liver peroxisomal beta-oxidation of feeding diets containing various amounts of dietary oils was investigated. With increasing amounts (5-25%, w/w) of soya-bean oil an apparent, but not statistically significant, increase of 1.5-fold was found both in specific activity, and in total liver activity. Increasing amounts of partially hydrogenated marine oil revealed a sigmoidal dose-response-curve, giving a 4-6-fold increase in the peroxisomal beta-oxidation activity at 20% or more of this oil in the diet. 2. Addition of small amounts of soya-bean oil to the marine-oil diet had no effect on the peroxisomal beta-oxidation activity, but decreased the C20:3(5,8,11) fatty acid/C20:4(5,8,11,14) fatty acid ratio in liver phospholipids from 0.74 to 0.01. 3. Starvation for 2 days led to a 1.5-1.8-fold increase in the peroxisomal beta-oxidation activity in rats previously fed on a standard pelleted diet, but had no effect in rats given high-fat diets. 4. Feeding partially hydrogenated marine oil or partially hydrogenated rape-seed oil resulted in higher activities than the corresponding unhydrogenated oils. 5. No significant differences in the effect on peroxisomal beta-oxidation could be detected between diets containing rape-seed oils with 15 or 45% erucic acid respectively. 6. These findings are discussed in relation to the possible effects of C22:1 and trans fatty acids in the process leading to increased peroxisomal beta-oxidation activity in the liver.

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Effects of high-fat diets on hepatic fatty acid oxidation in the rat Isolation of rat liver peroxisomes by vertical-rotor centrifugation by using a self-generated, iso-osmotic, Percoll gradient

Biochemical Journal ◽

10.1042/bj1960149 ◽

1981 ◽

Vol 196 (1) ◽

pp. 149-159 ◽

Cited By ~ 139

Author(s):

C E Neat ◽

M S Thomassen ◽

H Osmundsen

Keyword(s):

Fatty Acids ◽

Fatty Acid ◽

Rat Liver ◽

Unsaturated Fatty Acids ◽

High Fat ◽

Beta Oxidation ◽

Vertical Rotor ◽

High Fat Diets ◽

Fat Diets ◽

Long Chain

1. Rat liver peroxisomal fractions were isolated in iso-osmotic Percoll gradients by using vertical-rotor centrifugation. The fractions obtained with rats given various dietary treatments were characterized. 2. The effect on peroxisomal beta-oxidation of feeding 15% by wt. of dietary fat for 3 weeks was investigated. High-fat diets caused induction of peroxisomal beta-oxidation, but diets rich in very-long-chain mono-unsaturated fatty acids produced a more marked induction. 3. Peroxisomal beta-oxidation induced by diets rich in very-long-chain mono-unsaturated fatty acids can oxidize such acids. Trans-isomers of mono-unsaturated fatty acids are oxidized at rates that are faster than, or similar to, those obtained with corresponding cis-isomers. 4. Rates of oxidation of [14-14C]erucic acid by isolated rat hepatocytes isolated from rats fed on high-fat diets increased with the time on those diets in a fashion very similar to that previously reported for peroxisomal beta-oxidation [see Neat, Thomassen & Osmundsen (1980) Biochem, J. 186, 369-371]. 5. Total liver capacities for peroxisomal beta-oxidation (expressed as acetyl groups produced per min) were estimated to range from 10 to 30% of mitochondrial capacities, depending on dietary treatment and fatty acid substrate. A role is proposed for peroxisomal beta-oxidation in relation to the metabolism of fatty acids that are poorly oxidized by mitochondrial beta-oxidation, and, in general, as regards oxidation of fatty acids during periods of sustained high hepatic influx of fatty acids.

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Acute Toxicity of Acrylonitrile: Effect of Diet on Tissue Nonprotein Sulfhydryl Content and Distribution of 1–14C-Acrylonitrile or Its Metabolites

Journal of the American College of Toxicology ◽

10.3109/10915818409009076 ◽

1984 ◽

Vol 3 (1) ◽

pp. 93-102 ◽

Cited By ~ 4

Author(s):

R. J. Jaeger ◽

I. L. Cote ◽

A. E. Rogers ◽

E. H. Silver ◽

S. Szabo

Keyword(s):

Acute Toxicity ◽

High Fat Diet ◽

Specific Activity ◽

Control Diet ◽

Saturated Fat ◽

Standard Laboratory ◽

High Fat ◽

Complete Diet ◽

High Fat Diets ◽

Fat Diets

The influence of diet on the acute toxicity (lethality) and distribution of glutathione as measured by tissue nonprotein sulfhydryl (NPSH) concentration following acrylonitrile (ACN) treatment was studied. The tissue distribution of radiolabeled (14C) acrylonitrile or its radioactive metabolites was also determined. The diets tested were a standard laboratory rat chow; a casein-based, complete diet; and 2 diets high in saturated fat content that were either lipotrope deficient or lipotrope supplemented. The latter 2 diets were associated with decreased weight gain in the absence of ACN and increased lethality after orally administratered ACN. The increase in lethality, while most pronounced in the group fed the lipotrope-deficient, high-fat diet, was also seen in rats fed the purified control diet. The high-fat diets were associated with increases in brain and liver NPSH concentrations (mg NPSH/100 g body weight). Following oral administration of 1–14C-ACN, blood contained the highest specific activity. In terms of fraction of administered dose, liver was found to contain the highest total fraction. In the tissues measured, a majority of radioactivity appeared bound to trichloroacetic acid (TCA) insoluble components. The sequence of tissue activity (nCi 14C per g or ml) was as follows: blood > stomach > liver, duodenum, lung, kidney > brain > adrenal. While diet affected toxicity, it did not modify this general ranking.

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Non-Fasting Factor VII Coagulant Activity (FVII:C) Increased by High-Fat Diet

Thrombosis and Haemostasis ◽

10.1055/s-0038-1642518 ◽

1994 ◽

Vol 71 (06) ◽

pp. 755-758 ◽

Cited By ~ 46

Author(s):

E M Bladbjerg ◽

P Marckmann ◽

B Sandström ◽

J Jespersen

Keyword(s):

High Fat Diet ◽

Fat Content ◽

Factor Vii ◽

Amidolytic Activity ◽

High Fat ◽

Low Fat Diet ◽

Increased Risk ◽

Coagulant Activity ◽

High Fat Diets ◽

Fat Diets

SummaryPreliminary observations have suggested that non-fasting factor VII coagulant activity (FVII:C) may be related to the dietary fat content. To confirm this, we performed a randomised cross-over study. Seventeen young volunteers were served 2 controlled isoenergetic diets differing in fat content (20% or 50% of energy). The 2 diets were served on 2 consecutive days. Blood samples were collected at 8.00 h, 16.30 h and 19.30 h, and analysed for triglycerides, FVII coagulant activity using human (FVII:C) or bovine thromboplastin (FVII:Bt), and FVII amidolytic activity (FVIPAm). The ratio FVII:Bt/FVII:Am (a measure of FVII activation) increased from fasting levels on both diets, but most markedly on the high-fat diet. In contrast, FVII: Am (a measure of FVII protein) tended to decrease from fasting levels on both diets. FVII:C rose from fasting levels on the high-fat diet, but not on the low-fat diet. The findings suggest that high-fat diets increase non-fasting FVII:C, and consequently may be associated with increased risk of thrombosis.

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