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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 oxidative modification of protein and lipid.(A) Liver lipid peroxide (LPO) levels were determined at the times indicated. Each point represents the mean ± SD for 4 liver samples. (B) DNP-derivatized liver tissue lysates (lanes+) from control, HF or HF+KO-fed rats were analysed for the presence of oxidized protein. DNP protein bands were visualized by chemiluminescence. Oxyblot images were analyzed by densitometry and the values reported in the graph represent the means ± SD (n = 4). The amount of carbonylated proteins revealed at the beginning of dietary treatment was set to 100%. *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
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pone-0038797-g007: Effect of KO on oxidative modification of protein and lipid.(A) Liver lipid peroxide (LPO) levels were determined at the times indicated. Each point represents the mean ± SD for 4 liver samples. (B) DNP-derivatized liver tissue lysates (lanes+) from control, HF or HF+KO-fed rats were analysed for the presence of oxidized protein. DNP protein bands were visualized by chemiluminescence. Oxyblot images were analyzed by densitometry and the values reported in the graph represent the means ± SD (n = 4). The amount of carbonylated proteins revealed at the beginning of dietary treatment was set to 100%. *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.

Mentions: It has been reported that a dysfunction of the mitochondrial oxidative phosphorylation may represent one of the causes responsible for the increase of reactive oxygen species (ROS) [29]. ROS, in turn, may oxidatively modify cellular protein and lipid, thereby leading to the appearance of several pathologies. The oxidative damage of hepatic lipids is shown in Fig. 7A. Whereas the lipid peroxide (LPO) levels were identical in both control and HF+KO rats at any time, a significant increase (+19%) was found in the HF animals after 12 weeks of treatment. The analysis of protein oxidation in liver (Fig. 7B) revealed a strong increase in the level of oxidized proteins in HF animals at 8 (+38%) and 12 (+65%) weeks of dietary treatment (Fig. 7B). On the contrary, the values found in HF+KO rats at the 4th, 6th, and 8th week were only slightly increased in comparison to those measured in control animals. At the 12th week of dietary treatment no significant difference in the oxidative modification of protein was detected between the HF+KO and the control group of animals (Fig. 7B). It appears, therefore, that the HF diet is able to increase the oxidative damage of both proteins and lipids, expecially at longer feeding periods, and that this effect is efficiently reversed by KO supplementation of the HF diet.


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 oxidative modification of protein and lipid.(A) Liver lipid peroxide (LPO) levels were determined at the times indicated. Each point represents the mean ± SD for 4 liver samples. (B) DNP-derivatized liver tissue lysates (lanes+) from control, HF or HF+KO-fed rats were analysed for the presence of oxidized protein. DNP protein bands were visualized by chemiluminescence. Oxyblot images were analyzed by densitometry and the values reported in the graph represent the means ± SD (n = 4). The amount of carbonylated proteins revealed at the beginning of dietary treatment was set to 100%. *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3369862&req=5

pone-0038797-g007: Effect of KO on oxidative modification of protein and lipid.(A) Liver lipid peroxide (LPO) levels were determined at the times indicated. Each point represents the mean ± SD for 4 liver samples. (B) DNP-derivatized liver tissue lysates (lanes+) from control, HF or HF+KO-fed rats were analysed for the presence of oxidized protein. DNP protein bands were visualized by chemiluminescence. Oxyblot images were analyzed by densitometry and the values reported in the graph represent the means ± SD (n = 4). The amount of carbonylated proteins revealed at the beginning of dietary treatment was set to 100%. *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
Mentions: It has been reported that a dysfunction of the mitochondrial oxidative phosphorylation may represent one of the causes responsible for the increase of reactive oxygen species (ROS) [29]. ROS, in turn, may oxidatively modify cellular protein and lipid, thereby leading to the appearance of several pathologies. The oxidative damage of hepatic lipids is shown in Fig. 7A. Whereas the lipid peroxide (LPO) levels were identical in both control and HF+KO rats at any time, a significant increase (+19%) was found in the HF animals after 12 weeks of treatment. The analysis of protein oxidation in liver (Fig. 7B) revealed a strong increase in the level of oxidized proteins in HF animals at 8 (+38%) and 12 (+65%) weeks of dietary treatment (Fig. 7B). On the contrary, the values found in HF+KO rats at the 4th, 6th, and 8th week were only slightly increased in comparison to those measured in control animals. At the 12th week of dietary treatment no significant difference in the oxidative modification of protein was detected between the HF+KO and the control group of animals (Fig. 7B). It appears, therefore, that the HF diet is able to increase the oxidative damage of both proteins and lipids, expecially at longer feeding periods, and that this effect is efficiently reversed by KO supplementation of the HF diet.

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