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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 protein levels of mitochondrial CIC.Liver mitochondrial proteins from control, HF or HF+KO-fed rats were separated by SDS-PAGE, transferred to nitrocellulose and then immunodecorated with antisera against either the rat CIC or the mammalian porin. The values reported in the graph represent the means ± SD (n = 4; *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet). The amount of CIC revealed by immunodecoration at the beginning of dietary treatment was set to 100%.
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pone-0038797-g003: Effect of KO on protein levels of mitochondrial CIC.Liver mitochondrial proteins from control, HF or HF+KO-fed rats were separated by SDS-PAGE, transferred to nitrocellulose and then immunodecorated with antisera against either the rat CIC or the mammalian porin. The values reported in the graph represent the means ± SD (n = 4; *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet). The amount of CIC revealed by immunodecoration at the beginning of dietary treatment was set to 100%.

Mentions: Furthermore, the kinetic properties of the CIC activity were investigated in the proteoliposomal system. No significant difference was found in the Km values for the reconstituted CIC activity in the three groups of rats (Table 2). On the contrary, a net decrease in the Vmax values was found in the HF+KO group with respect to both the control and the HF group. In good agreement with the above mentioned results (Fig. 2A and B), a similar extent of inhibition (about 67%) was found in the case of Vmax after 12 weeks of dietary treatment. These findings were fully validated by western blot experiments in which the expression of the mitochondrial CIC was monitored over time in the three treatment groups. The decrease in the CIC activity found in the HF+KO rats was accompanied by a strong decrease in the amount of the mitochondrial carrier protein in the same group of animals (Fig. 3). After 12 weeks of HF+KO dietary treatment the amount of mitochondrial CIC decreased 55%, compared to control and HF groups. Interestingly, a small, although significant, decrease in the amount of CIC protein was also found at the 4th week in the HF group in comparison to the control group. These results suggest that the CIC inhibition due to KO supplementation of the HF diet depends on a strong decrease in the expression of this mitochondrial carrier protein. The amount of porin, an outer membrane protein tested as a control, did not change in any group at any time of treatment.


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 protein levels of mitochondrial CIC.Liver mitochondrial proteins from control, HF or HF+KO-fed rats were separated by SDS-PAGE, transferred to nitrocellulose and then immunodecorated with antisera against either the rat CIC or the mammalian porin. The values reported in the graph represent the means ± SD (n = 4; *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet). The amount of CIC revealed by immunodecoration at the beginning of dietary treatment was set to 100%.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3369862&req=5

pone-0038797-g003: Effect of KO on protein levels of mitochondrial CIC.Liver mitochondrial proteins from control, HF or HF+KO-fed rats were separated by SDS-PAGE, transferred to nitrocellulose and then immunodecorated with antisera against either the rat CIC or the mammalian porin. The values reported in the graph represent the means ± SD (n = 4; *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet). The amount of CIC revealed by immunodecoration at the beginning of dietary treatment was set to 100%.
Mentions: Furthermore, the kinetic properties of the CIC activity were investigated in the proteoliposomal system. No significant difference was found in the Km values for the reconstituted CIC activity in the three groups of rats (Table 2). On the contrary, a net decrease in the Vmax values was found in the HF+KO group with respect to both the control and the HF group. In good agreement with the above mentioned results (Fig. 2A and B), a similar extent of inhibition (about 67%) was found in the case of Vmax after 12 weeks of dietary treatment. These findings were fully validated by western blot experiments in which the expression of the mitochondrial CIC was monitored over time in the three treatment groups. The decrease in the CIC activity found in the HF+KO rats was accompanied by a strong decrease in the amount of the mitochondrial carrier protein in the same group of animals (Fig. 3). After 12 weeks of HF+KO dietary treatment the amount of mitochondrial CIC decreased 55%, compared to control and HF groups. Interestingly, a small, although significant, decrease in the amount of CIC protein was also found at the 4th week in the HF group in comparison to the control group. These results suggest that the CIC inhibition due to KO supplementation of the HF diet depends on a strong decrease in the expression of this mitochondrial carrier protein. The amount of porin, an outer membrane protein tested as a control, did not change in any group at any time of treatment.

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