Polyunsaturated n-3 and n-6 fatty acids at a low level in the diet alter mitochondrial outer membrane parameters in Wistar rat liver

Clouet, Pierre; Niot, Isabelle; Gresti, Joseph; Demarquoy, Jean; Boichot, Jacqueline; Durand, Georges; Bézard, J.

doi:10.1016/0955-2863(95)00123-h

Cited by 5 publications

(7 citation statements)

References 44 publications

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“…This may be explained at least from two parameters: (1) as the FA composition of mithchondrial outer membranes was reported to be influenced by the dietary FA (Berger et al. 1992; Clouet et al. 1995), the increase in dietary PUFA supplied to rats was sufficient to influence the content of n‐3 and n‐6 PUFAs in mitochondrial outer membranes and to alter some of the characteristics of CPT I (Clouet et al.…”

Section: Discussionmentioning

confidence: 99%

Utilization of different dietary lipid sources at high level in herbivorous grass carp (Ctenopharyngodon idella): mechanism related to hepatic fatty acid oxidation

Clouet

Huang

et al. 2008

Aquaculture Nutrition

205

125

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Herbivorous grass carp (Ctenopharyngodon idella) has been reported to exhibit low capacity to utilize high dietary lipid, but different lipid sources might affect this limited capacity. In order to compare the effects of different lipid sources with different lipid levels, juvenile grass carp were fed one of nine diets containing three oils [lard, plant oil mixed by maize and linseed oil, and n‐3 high unsaturated fatty acid‐enriched (HUFA‐enriched) fish oil] at three lipid levels (20, 60 and 100 g kg−1 dry diet) for 8 weeks. Decreased feed intake, poor growth performance, hepatic pathology and higher blood lipid peroxidation were found in 60 and 100 g kg−1 fish oil groups. Conversely, in lard and plant oil groups, even at 100 g kg−1 dietary lipid level, feed intake and growth performance did not decrease, despite histological observation revealed hepatic pathology in these groups. Plasma triglyceride and cholesterol contents increased significantly in all 100 g kg−1 dietary lipid groups. In the comparison of hepatic FA β‐oxidation among three oil groups at 60 g kg−1 dietary lipid level, impaired mitochondrial and peroxisomal FA oxidation capacity was observed in fish oil group. The results confirmed the relatively low capacity of grass carp to utilize high dietary lipid, and furthermore excess HUFA intake will result in more serious adverse effects than other FA.

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Section: Discussionmentioning

confidence: 99%

Utilization of different dietary lipid sources at high level in herbivorous grass carp (Ctenopharyngodon idella): mechanism related to hepatic fatty acid oxidation

Clouet

Huang

et al. 2008

Aquaculture Nutrition

205

125

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“…17,18 Although fat intake 19,20 and genotype 21,22 interact to regulate fat deposition, there are both in vitro 1,23 and in vivo 24,25 data which suggest that dietary fatty acid composition modulates to some extent the partitioning of fat between oxidation and storage.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, ®sh oil has been shown to enhance carnitine palmitoyltransferase I activity in rats, 30 mice 31 and Syrian hamsters, 32 and to decrease the sensitivity of carnitine palmitoyltransferase I to malonyl-CoA inhibition in liver mitochondria 33 even in rats fed ®sh oil at a level as low as 0.2% of the diet. 1 It should be noted that any increase in the carnitine palmitoyltransferase I activity and/or reduction in its malonyl-CoA inhibition renders fatty acids more available for the b-oxidative pathway. Whether ®sh oil can affect carnitine palmitoyltransferase activity or lipid oxidation in tissues other than liver is not known.…”

Section: Discussionmentioning

confidence: 99%

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Effect of dietary fish oil on body fat mass and basal fat oxidation in healthy adults

et al. 1997

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OBJECTIVE: To investigate whether the substitution of ®sh oil for visible fats in a control diet (52% carbohydrates, 16% protein, 32% fat; P:S 0.2) in¯uences body fat mass and substrate oxidation in healthy adults. DESIGN: Six volunteers (5 men; 23 AE 2 y; BMI: 21.9 AE 1.6) were fed a control diet (C) ad libitum during a period of three weeks and, 10±12 weeks later, the same diet where 6 g/d of visible fat were replaced by 6 g/d of ®sh oil (FO) for another three weeks. RESULTS: Energy intakes (IKA-calorimeter) were unchanged. Body fat mass (Dual-energy X-ray absorptiometry) decreased with FO (70.88 AE 0.16 vs 70.3 AE 0.34 kg; FO vs C; P`0.05). When adjusted for lean body mass (Ancova), resting metabolic rate (indirect calorimetry) was unchanged. Basal respiratory quotient decreased with FO (0.815 AE 0.02 vs 0.834 AE 0.02; P`0.05) and basal lipid oxidation increased with FO (1.06 AE 0.17 vs 0.87 AE 0.13 mg kg 71 min 71 ; P`0.05). CONCLUSION: Dietary FO reduces body fat mass and stimulates lipid oxidation in healthy adults.

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“…They were then extracted for total lipids according to Folch et al (22) after addition of 1,2,3-triheptadecanoylglycerol and pentadecanoic acid, as internal standards for TG and free FA (FFA) determinations, respectively. Lipid classes were separated by thin-layer chromatography on silica gel and measured after gas liquid chromatography of constitutive FA methyl esters (23).…”

Section: Liver Secretion and Palmitate Perfusionmentioning

confidence: 99%

Regulation of Lipid Flux between Liver and Adipose Tissue during Transient Hepatic Steatosis in Carnitine-depleted Rats

Degrace

Demizieux

et al. 2007

Journal of Biological Chemistry

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Rats with carnitine deficiency due to trimethylhydrazinium propionate (mildronate) administered at 80 mg/100 g body weight per day for 10 days developed liver steatosis only upon fasting. This study aimed to determine whether the transient steatosis resulted from triglyceride accumulation due to the amount of fatty acids preserved through impaired fatty acid oxidation and/or from upregulation of lipid exchange between liver and adipose tissue. In liver, mildronate decreased the carnitine content by ϳ13-fold and, in fasted rats, lowered the palmitate oxidation rate by 50% in the perfused organ, increased 9-fold the triglyceride content, and doubled the hepatic very low density lipoprotein secretion rate. Concomitantly, triglyceridemia was 13-fold greater than in controls. Hepatic carnitine palmitoyltransferase I activity and palmitate oxidation capacities measured in vitro were increased after treatment. Gene expression of hepatic proteins involved in fatty acid oxidation, triglyceride formation, and lipid uptake were all increased and were associated with increased hepatic free fatty acid content in treated rats. In periepididymal adipose tissue, mildronate markedly increased lipoprotein lipase and hormone-sensitive lipase activities in fed and fasted rats, respectively. On refeeding, carnitine-depleted rats exhibited a rapid decrease in blood triglycerides and free fatty acids, then after ϳ2 h, a marked drop of liver triglycerides and a progressive decrease in liver free fatty acids. Data show that up-regulation of liver activities, peripheral lipolysis, and lipoprotein lipase activity were likely essential factors for excess fat deposit and release alternately occurring in liver and adipose tissue of carnitine-depleted rats during the fed/fasted transition.Fat is mainly deposited in adipose tissue, but is also observed in liver biopsies of humans suffering from disorders originating, for instance, from alcohol abuse, diabetes (1), or intoxications (2). Fat storage usually results from the imbalance of the partitioning of lipids between their utilization as energy sources and their preservation or synthesis as triglycerides (TG) 2 initially provided by excess feeding or increased lipogenesis (3). Liver steatosis may also exist when the lipoprotein secretion mechanisms are impaired (4, 5). Genetic models of animal obesity (6, 7) and overweight humans (8, 9) have provided information on regulations occurring in adipose tissue and liver, in which fat deposit may be the consequence of actions mediated by insulin, such as inhibition of fatty acid (FA) oxidation (10) or increased lipogenesis (11,12), and even of hypothalamic injuries (13). Experimental studies have been undertaken to amplify the inhibition of the FA oxidation pathway with drugs that reduce the carnitine-dependent transfer of FA into mitochondria, for example, etomoxir for the carnitine palmitoyltransferase (CPT) I step (14), L-aminocarnitine for the CPT II step (15), or 3,2,2,2-trimethylhydrazinium propionate (mildronate) for liver carnitine biosynth...

show abstract

Polyunsaturated n-3 and n-6 fatty acids at a low level in the diet alter mitochondrial outer membrane parameters in Wistar rat liver

Cited by 5 publications

References 44 publications

Utilization of different dietary lipid sources at high level in herbivorous grass carp (Ctenopharyngodon idella): mechanism related to hepatic fatty acid oxidation

Utilization of different dietary lipid sources at high level in herbivorous grass carp (Ctenopharyngodon idella): mechanism related to hepatic fatty acid oxidation

Effect of dietary fish oil on body fat mass and basal fat oxidation in healthy adults

Regulation of Lipid Flux between Liver and Adipose Tissue during Transient Hepatic Steatosis in Carnitine-depleted Rats

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