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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 cholesterol and phospholipid contents in liver mitochondria.The levels of liver cholesterol (A) and cholesterol/phospholipids ratio (B) were determined at the times indicated. Each point represents the mean ± SD (n = 3). *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
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pone-0038797-g010: Effect of KO on cholesterol and phospholipid contents in liver mitochondria.The levels of liver cholesterol (A) and cholesterol/phospholipids ratio (B) were determined at the times indicated. Each point represents the mean ± SD (n = 3). *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.

Mentions: Cholesterol and phospholipid contents of mitochondrial membranes from control and treated animals were analyzed. No significant difference was observed in the phospholipid concentration and composition of hepatic rat mitochondria in the three groups (data not shown). However, after 8 weeks of treatment, cholesterol content of mitochondrial membranes was affected upon HF and HF+KO treatments. There was a strong increase in the level of cholesterol in HF animals after 8 (+35%) and 12 (+78%) weeks of dietary treatment, in comparison to the values found in control animals (Fig. 10A). On the contrary, the values found in HF+KO rats were lower than those of the control group (20% and 34% decrease after 8 and 12 weeks, respectively). Accordingly, the cholesterol/phospholipid ratio was significantly higher in the liver mitochondria from HF rats in comparison to the control, whereas a strong reduction in this parameter was observed in the HF+KO group (Fig. 10B).


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 cholesterol and phospholipid contents in liver mitochondria.The levels of liver cholesterol (A) and cholesterol/phospholipids ratio (B) were determined at the times indicated. Each point represents the mean ± SD (n = 3). *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-g010: Effect of KO on cholesterol and phospholipid contents in liver mitochondria.The levels of liver cholesterol (A) and cholesterol/phospholipids ratio (B) were determined at the times indicated. Each point represents the mean ± SD (n = 3). *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
Mentions: Cholesterol and phospholipid contents of mitochondrial membranes from control and treated animals were analyzed. No significant difference was observed in the phospholipid concentration and composition of hepatic rat mitochondria in the three groups (data not shown). However, after 8 weeks of treatment, cholesterol content of mitochondrial membranes was affected upon HF and HF+KO treatments. There was a strong increase in the level of cholesterol in HF animals after 8 (+35%) and 12 (+78%) weeks of dietary treatment, in comparison to the values found in control animals (Fig. 10A). On the contrary, the values found in HF+KO rats were lower than those of the control group (20% and 34% decrease after 8 and 12 weeks, respectively). Accordingly, the cholesterol/phospholipid ratio was significantly higher in the liver mitochondria from HF rats in comparison to the control, whereas a strong reduction in this parameter was observed in the HF+KO group (Fig. 10B).

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