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A krill oil supplemented diet suppresses hepatic steatosis in high-fat fed rats.

Ferramosca A, Conte A, Burri L, Berge K, De Nuccio F, Giudetti AM, Zara V - PLoS ONE (2012)

Bottom Line: This effect was accompanied by a parallel reduction of the plasma levels of triglycerides and glucose and by the prevention of a plasma insulin increase.The investigation of the molecular mechanisms of KO action in high-fat fed animals revealed a strong decrease in the activities of the mitochondrial citrate carrier and of the cytosolic acetyl-CoA carboxylase and fatty acid synthetase, which are both involved in hepatic de novo lipogenesis.Lastly, the KO supplementation prevented an increase in body weight, as well as oxidative damage of lipids and proteins, which is often found in high-fat fed animals.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological and Environmental Sciences and Technologies, University of Salento, Lecce, Italy.

ABSTRACT
Krill oil (KO) is a dietary source of n-3 polyunsaturated fatty acids, mainly represented by eicosapentaenoic acid and docosahexaenoic acid bound to phospholipids. The supplementation of a high-fat diet with 2.5% KO efficiently prevented triglyceride and cholesterol accumulation in liver of treated rats. This effect was accompanied by a parallel reduction of the plasma levels of triglycerides and glucose and by the prevention of a plasma insulin increase. The investigation of the molecular mechanisms of KO action in high-fat fed animals revealed a strong decrease in the activities of the mitochondrial citrate carrier and of the cytosolic acetyl-CoA carboxylase and fatty acid synthetase, which are both involved in hepatic de novo lipogenesis. In these animals a significant increase in the activity of carnitine palmitoyl-transferase I and in the levels of carnitine was also observed, suggesting a concomitant stimulation of hepatic fatty acid oxidation. The KO supplemented animals also retained an efficient mitochondrial oxidative phosphorylation, most probably as a consequence of a KO-induced arrest of the uncoupling effects of a high-fat diet. Lastly, the KO supplementation prevented an increase in body weight, as well as oxidative damage of lipids and proteins, which is often found in high-fat fed animals.

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Related in: MedlinePlus

Effect of KO on body weight.Body weights of rats fed control (filled circle), HF (open circle) and HF+KO (filled square) diets are indicated for the treatment periods in weeks. Each point represents the mean ± SD for 10 animals. *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
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pone-0038797-g001: Effect of KO on body weight.Body weights of rats fed control (filled circle), HF (open circle) and HF+KO (filled square) diets are indicated for the treatment periods in weeks. Each point represents the mean ± SD for 10 animals. *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.

Mentions: Animals (male Sprague-Dawley rats) were randomly divided into three groups and fed a control diet, a HF diet or a HF+KO diet for 12 weeks (Table 1). The food intake did not differ significantly between the three treatment groups during the study (Control group: 11.8±1.8 g/die; HF group: 12.4±0.7 g/die; HF+KO group: 11.8±1.4 g/die). On the contrary, a significant increase in body weight of rats belonging to the HF group was detectable already after 4 weeks of treatment, in comparison to control animals (Fig. 1). This finding was predictable on the basis of the higher caloric content of the HF diet with respect to the standard diet (Table 1). Interestingly, the supplementation of the HF diet with 2.5% KO (HF+KO group) significantly prevented this effect (Fig. 1). The liver weight did not differ significantly between the three groups at any time during the dietary treatment (data not shown).


A krill oil supplemented diet suppresses hepatic steatosis in high-fat fed rats.

Ferramosca A, Conte A, Burri L, Berge K, De Nuccio F, Giudetti AM, Zara V - PLoS ONE (2012)

Effect of KO on body weight.Body weights of rats fed control (filled circle), HF (open circle) and HF+KO (filled square) diets are indicated for the treatment periods in weeks. Each point represents the mean ± SD for 10 animals. *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3369862&req=5

pone-0038797-g001: Effect of KO on body weight.Body weights of rats fed control (filled circle), HF (open circle) and HF+KO (filled square) diets are indicated for the treatment periods in weeks. Each point represents the mean ± SD for 10 animals. *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
Mentions: Animals (male Sprague-Dawley rats) were randomly divided into three groups and fed a control diet, a HF diet or a HF+KO diet for 12 weeks (Table 1). The food intake did not differ significantly between the three treatment groups during the study (Control group: 11.8±1.8 g/die; HF group: 12.4±0.7 g/die; HF+KO group: 11.8±1.4 g/die). On the contrary, a significant increase in body weight of rats belonging to the HF group was detectable already after 4 weeks of treatment, in comparison to control animals (Fig. 1). This finding was predictable on the basis of the higher caloric content of the HF diet with respect to the standard diet (Table 1). Interestingly, the supplementation of the HF diet with 2.5% KO (HF+KO group) significantly prevented this effect (Fig. 1). The liver weight did not differ significantly between the three groups at any time during the dietary treatment (data not shown).

Bottom Line: This effect was accompanied by a parallel reduction of the plasma levels of triglycerides and glucose and by the prevention of a plasma insulin increase.The investigation of the molecular mechanisms of KO action in high-fat fed animals revealed a strong decrease in the activities of the mitochondrial citrate carrier and of the cytosolic acetyl-CoA carboxylase and fatty acid synthetase, which are both involved in hepatic de novo lipogenesis.Lastly, the KO supplementation prevented an increase in body weight, as well as oxidative damage of lipids and proteins, which is often found in high-fat fed animals.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological and Environmental Sciences and Technologies, University of Salento, Lecce, Italy.

ABSTRACT
Krill oil (KO) is a dietary source of n-3 polyunsaturated fatty acids, mainly represented by eicosapentaenoic acid and docosahexaenoic acid bound to phospholipids. The supplementation of a high-fat diet with 2.5% KO efficiently prevented triglyceride and cholesterol accumulation in liver of treated rats. This effect was accompanied by a parallel reduction of the plasma levels of triglycerides and glucose and by the prevention of a plasma insulin increase. The investigation of the molecular mechanisms of KO action in high-fat fed animals revealed a strong decrease in the activities of the mitochondrial citrate carrier and of the cytosolic acetyl-CoA carboxylase and fatty acid synthetase, which are both involved in hepatic de novo lipogenesis. In these animals a significant increase in the activity of carnitine palmitoyl-transferase I and in the levels of carnitine was also observed, suggesting a concomitant stimulation of hepatic fatty acid oxidation. The KO supplemented animals also retained an efficient mitochondrial oxidative phosphorylation, most probably as a consequence of a KO-induced arrest of the uncoupling effects of a high-fat diet. Lastly, the KO supplementation prevented an increase in body weight, as well as oxidative damage of lipids and proteins, which is often found in high-fat fed animals.

Show MeSH
Related in: MedlinePlus