Effects of a fish oil-lard diet on rat plasma lipoproteins, liver FAS, and lipolytic enzymes

Benhizia, Ferdaous; Hainault, Isabelle; Sérougne, Colette; Lagrange, Dominique; Hajduch, Éric; Guichard, C; Malewiak, Marie-Irène; Quignard‐Boulangé, Annie; Lavau, M; Griglio, S.

doi:10.1152/ajpendo.1994.267.6.e975

Cited by 33 publications

(37 citation statements)

References 37 publications

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“…24 Indeed, mice in the present study fed the HF/FO diet showed reduced hepatic gene expression levels of lipogenic enzymes Srebp-1c, Acc1, Acc2 and Fasn compared with those observed in the HF group. In addition, the rate of lipid oxidation assessed by indirect calorimetry was clearly highest in the HF/FO group.…”

Section: Discussionmentioning

confidence: 46%

“…22 Thus, while a high-saturated-fat diet stimulates the expression of genes encoding lipogenic enzymes in the liver, such as Srebp-1c and Fasn expression, 23 a diet with a high content of poly-unsaturated fatty acids (PUFAs) has the opposite effects. 24,25 Since changes in lipid fluxes are suggested to be, at least in part, responsible for the antiobesity effect of rimonabant treatment, it can be hypothesized that efficacy of rimonabant treatment may depend on changes in lipid fluxes resulting from differences in dietary fat composition. Up till now, relatively little attention has been paid to the role of dietary fat composition in relation to the efficacy of rimonabant treatment.…”

Section: Introductionmentioning

confidence: 99%

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Metabolic responses to long-term pharmacological inhibition of CB1-receptor activity in mice in relation to dietary fat composition

et al. 2009

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Background and objectives:The antiobesity effects of suppressed endocannabinoid signaling may rely, at least in part, on changes in lipid fluxes. As fatty acids exert specific effects depending on their level of saturation, we hypothesized that the dietary fatty acid composition would influence the outcome of treatment with a CB 1 -receptor antagonist (rimonabant). Methods: Mice were treated with rimonabant (10 mg kg À1 body weight per day) or vehicle while equicalorically fed either a low-fat diet (LF), a high-fat (HF) diet or an HF diet in which 10% of the saturated fatty acids (SFAs) were replaced by polyunsaturated fatty acids (PUFA) from fish oil (FO). Food intake and body weight were registered daily. Indirect calorimetry was performed and feces were collected. After 3 weeks, mice were killed for blood and tissue collection. Results: Relative to the LF diet, the HF diet caused anticipated metabolic derangements, which were partly reversed by the HF/FO diet. The HF/FO diet, however, was most obesity-promoting despite inhibiting lipogenesis as indicated by low gene expression levels of lipogenic enzymes. On all three diets, rimonabant treatment improved metabolic derangements and led to significantly lower body weight gain than their respective controls. This latter effect appeared largest in the HF/FO group, but occurred without major changes in nutrient absorption and energy expenditure. Conclusion: The effects of chronic rimonabant treatment on body weight gain occurred irrespective of diet-induced changes in lipogenic activity, food intake and daily energy expenditure, and were, in fact, most pronounced in HF/FO mice. The effects of dietary PUFA replacement in an HF diet on expansion of adipose tissue might allow the favorable effects of dietary PUFA on dyslipidemia and hepatic steatosis. In light of other disadvantageous effects of weight gain, this might be a risky trade-off.

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Section: Discussionmentioning

confidence: 46%

Section: Introductionmentioning

confidence: 99%

Metabolic responses to long-term pharmacological inhibition of CB1-receptor activity in mice in relation to dietary fat composition

et al. 2009

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“…29) Previous studies have shown that the development of hypertriglyceridemia is closely associated with the downregulation of LPL activity. 30) In our research, however, the activity of plasma LPL was upregulated by a high-fat diet in both guinea pigs and rats, a result which could be induced by increasing exogenous TG synthesis in response to dietary fat. In any case, this result suggests that the hypertriglyceridemia in guinea pigs fed a high-fat diet may not result from downregulation of LPL activity.…”

Section: Discussioncontrasting

confidence: 53%

Hyperlipidemic Guinea Pig Model: Mechanisms of Triglyceride Metabolism Disorder and Comparison to Rat

Yang

Guo

Song

et al. 2011

Biological & Pharmaceutical Bulletin

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Hyperlipidemia is an important risk factor for coronary heart disease. A proper animal model plays vital roles in the researches on mechanisms of lipid disorder. The advantages of using guinea pigs for cholesterol and lipoprotein metabolism investigations have been elucidated in many studies. The guinea pig is a suitable animal model for studying hyperlipidemia because of its similarities to humans in transporting the majority of its circulating cholesterol in low-density lipoprotein (LDL), exhibiting moderate rates of hepatic cholesterol synthesis and catabolism, having higher concentrations of free compared to esterified cholesterol in the liver and in many other aspects of lipid metabolism. [1][2][3][4][5] To date, however, little attention has been paid to triglyceride metabolism in guinea pigs.Rats have commonly been used for hyperlipidemia studies in the past, although their use has recently been in decline. They transport most of their serum cholesterol in the highdensity lipoprotein (HDL) fraction, have higher ability of plasma cholesterol clearance and couldn't develope a hypertriglyceridemia response to cholesterol feeding. More and more researchers indicated that the mechanisms by which diet interventions and drug treatments alter plasma lipids and lipoprotein metabolism in rats are different from humans. [6][7][8][9] In our previous studies, we also found that a high-fat diet containing 0.1% cholesterol and 10% lard induced typical hyperlipidemia and hypertriglyceridemia in guinea pigs but not in rats.10) And there is less number of good hypertriglyceridemic models. Therefore, it is very meaningful to further research the mechanisms of triglyceride metablism disorder in guinea pigs.The present study was designed to determine the comparative plasma and hepatic lipid responses of guinea pigs and rats to high-fat diets containing 0.1% cholesterol and 10% lard and to compare the enzyme activities and gene expression of molecules that closely related to triglyceride metabolism. MATERIALS AND METHODSReagents Acetyl-CoA, Triton WR-1339, malonyl-CoA, nicotinamide adenine dinucleotide phosphate (NADPH), DL-dithiothreitol (DTT), 5,5Ј-dithiobis(2-nitrobenzoate) (DTNB), palmitoyl-CoA, carnitine, 1,2-dipalmitoyl-sn-glycerol, palmitoyl-CoA lithium salt and glyceryl tripalmitate were purchased from Sigma-Aldrich. The solvents (chloroform, hexane, 2-propanol and methanol) were of HPLC grade (J. T. Baker, U.S.A.). All other reagents were of analytical grade and purchased from the Beijing Chemicals Company. The triglyceride (TG), total cholesterol (TC) and lowdensity lipoprotein cholesterol (LDL-C) assay kits were purchased from BioSino Bio-technology and Science, Inc. The lipoprotein lipase (LPL) and free fatty acids (FFA) kits were obtained from the Nanjing Jiancheng Bioengineering Institute. The RNApure high-purity total RNA rapid extraction kit, Super reverse transcription (RT) Kit (First Strand cDNA Synthesis Kit) and 2ϫSYBR real-time polymerase chain reaction (PCR) premixture were purchased from the BioTeke Corp...

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“…In this respect, the effects of several typical treatments such as administration of leptin, [57][58][59][60][61] bezafibrate, 62,63 adrenoreceptor agonists, 48,[64][65][66][67][68] dietary n-3 polyunsaturated FA [69][70][71] or fasting 66,[72][73][74] can be compared with a phenotype of the aP2-Ucp1 transgenic mice. 20,21,26 In all of these situations, fat accumulation is reduced and disturbances related to the metabolic syndrome are improved.…”

Section: Physiological Relevance Of Energy Metabolism and Ampk In Whimentioning

confidence: 99%

Role of energy charge and AMP-activated protein kinase in adipocytes in the control of body fat stores

et al. 2004

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As indicated by in vitro studies, both lipogenesis and lipolysis in adipocytes depend on the cellular ATP levels. Ectopic expression of mitochondrial uncoupling protein 1 (UCP1) in the white adipose tissue of the aP2-Ucp1 transgenic mice reduced obesity induced by genetic or dietary manipulations. Furthermore, respiratory uncoupling lowered the cellular energy charge in adipocytes, while the synthesis of fatty acids (FA) was inhibited and their oxidation increased. Importantly, the complex metabolic changes triggered by ectopic UCP1 were associated with the activation of AMP-activated protein kinase (AMPK), a metabolic master switch, in adipocytes. Effects of several typical treatments that reduce adiposity, such as administration of leptin, b-adrenoceptor agonists, bezafibrate, dietary n-3 polyunsaturated FA or fasting, can be compared with a phenotype of the aP2-Ucp1 mice. These situations generally lead to the upregulation of mitochondrial UCPs and suppression of the cellular energy charge and FA synthesis in adipocytes. On the other hand, FA oxidation is increased. Moreover, it has been shown that AMPK in adipocytes can be activated by adipocyte-derived hormones leptin and adiponectin, and also by insulin-sensitizes thiazolidinediones. Thus, it is evident that metabolism of adipose tissue itself is important for the control of body fat content and that the cellular energy charge and AMPK are involved in the control of lipid metabolism in adipocytes. The reciprocal link between synthesis and oxidation of FA in adipocytes represents a prospective target for the new treatment strategies aimed at reducing obesity.

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Effects of a fish oil-lard diet on rat plasma lipoproteins, liver FAS, and lipolytic enzymes

Cited by 33 publications

References 37 publications

Metabolic responses to long-term pharmacological inhibition of CB1-receptor activity in mice in relation to dietary fat composition

Metabolic responses to long-term pharmacological inhibition of CB1-receptor activity in mice in relation to dietary fat composition

Hyperlipidemic Guinea Pig Model: Mechanisms of Triglyceride Metabolism Disorder and Comparison to Rat

Role of energy charge and AMP-activated protein kinase in adipocytes in the control of body fat stores

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