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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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Effect of KO on liver lipids.(A) Cresyl violet staining of liver histological sections from rats fed for 12 weeks with control, HF or HF+KO diet. The levels of liver triglycerides (B) and cholesterol (C) were determined at the times indicated. Each point represents the mean ± SD for 4 liver samples. *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
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pone-0038797-g009: Effect of KO on liver lipids.(A) Cresyl violet staining of liver histological sections from rats fed for 12 weeks with control, HF or HF+KO diet. The levels of liver triglycerides (B) and cholesterol (C) were determined at the times indicated. Each point represents the mean ± SD for 4 liver samples. *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.

Mentions: Additionally, there were differences in lipid levels found in liver. The liver histologic examination revealed microvesicular fat depositions in HF rats, whereas no fat deposition was found in the HF+KO animals (Fig. 9A). After 12 weeks, the liver triglyceride content was 2.1 fold higher, compared to that in control animals. Interestingly, the KO supplementation of the HF diet reversed this effect, thereby assuring liver triglyceride levels very similar to those of control rats (Fig. 9B). Also the levels of total cholesterol significantly increased in HF rats in comparison to those of control animals (+77% after 12 weeks) (Fig. 9C). In the HF+KO animals, instead, the increase in cholesterol levels was significantly less evident being about +19% at the 12th week (Fig. 9C). The assay of liver phospholipid content did not reveal any significant difference among the various groups of animals at any time (data not shown). Accordingly, the dietary administration of KO in animals fed a HF diet has a normalizing effect on the hepatic content of both triglycerides and cholesterol.


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 liver lipids.(A) Cresyl violet staining of liver histological sections from rats fed for 12 weeks with control, HF or HF+KO diet. The levels of liver triglycerides (B) and cholesterol (C) were determined at the times indicated. Each point represents the mean ± SD for 4 liver samples. *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-g009: Effect of KO on liver lipids.(A) Cresyl violet staining of liver histological sections from rats fed for 12 weeks with control, HF or HF+KO diet. The levels of liver triglycerides (B) and cholesterol (C) were determined at the times indicated. Each point represents the mean ± SD for 4 liver samples. *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
Mentions: Additionally, there were differences in lipid levels found in liver. The liver histologic examination revealed microvesicular fat depositions in HF rats, whereas no fat deposition was found in the HF+KO animals (Fig. 9A). After 12 weeks, the liver triglyceride content was 2.1 fold higher, compared to that in control animals. Interestingly, the KO supplementation of the HF diet reversed this effect, thereby assuring liver triglyceride levels very similar to those of control rats (Fig. 9B). Also the levels of total cholesterol significantly increased in HF rats in comparison to those of control animals (+77% after 12 weeks) (Fig. 9C). In the HF+KO animals, instead, the increase in cholesterol levels was significantly less evident being about +19% at the 12th week (Fig. 9C). The assay of liver phospholipid content did not reveal any significant difference among the various groups of animals at any time (data not shown). Accordingly, the dietary administration of KO in animals fed a HF diet has a normalizing effect on the hepatic content of both triglycerides and cholesterol.

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