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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 the transport activity of mitochondrial CIC.Transport of citrate into rat liver mitochondria that are freshly isolated (A) and into a reconstituted system (proteoliposomes) (B) was measured at the times indicated. The values reported in the figure represent the means ± SD (n = 4). *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
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pone-0038797-g002: Effect of KO on the transport activity of mitochondrial CIC.Transport of citrate into rat liver mitochondria that are freshly isolated (A) and into a reconstituted system (proteoliposomes) (B) was measured at the times indicated. The values reported in the figure represent the means ± SD (n = 4). *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.

Mentions: The anabolic pathway of fatty acid synthesis utilizes the carbon units transported outside liver mitochondria by the CIC [19]. For this reason, we investigated the transport activity of this protein in freshly isolated mitochondria from liver of the three groups of rats. The transport activity of this mitochondrial carrier remained almost unaffected over time in the control group (Fig. 2A). Approximately the same trend was observed in the case of the HF group, i.e. almost no influence of the HF diet on the CIC activity over time. A small yet significant inhibition of the CIC activity in the HF group (about 12%) was only found after 4 weeks of dietary treatment (Fig. 2A). A net and significant decrease in the CIC activity was instead found in mitochondria isolated from the HF+KO group. After 12 weeks, such a decrease was 59% in the HF+KO group with respect to both control and HF groups. In this context, it is important to underline that the CIC protein operates in the inner mitochondrial membrane where it is deeply embedded. Therefore, its transport activity can be influenced, at least in principle, by the phospholipid and fatty acid composition of the inner mitochondrial membrane. In order to investigate this possibility, we extracted the CIC protein from the mitochondrial membranes using a non-denaturing detergent and subsequently purified it by hydroxyapatite chromatography. Eventually, the purified CIC was functionally reconstituted into liposomes, thereby obtaining the so-called proteoliposomes. The transport activity of the purified and reconstituted CIC from the HF+KO animals was significantly lower over time in comparison to that of both control and HF groups (Fig. 2B). An inhibition of about 60% was found at the 12th week of dietary treatment in HF+KO animals with respect to the other two groups of animals. Interestingly, the activity of the mitochondrial CIC in the rats of the HF group, excluding the inhibition observed after 4 weeks, was practically identical to that of the control rats (Fig. 2B). These observations imply that the addition of 2.5% KO to the HF diet (35% fat) is able to significantly decrease the transport activity of the mitochondrial CIC.


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 the transport activity of mitochondrial CIC.Transport of citrate into rat liver mitochondria that are freshly isolated (A) and into a reconstituted system (proteoliposomes) (B) was measured at the times indicated. The values reported in the figure represent the means ± SD (n = 4). *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-g002: Effect of KO on the transport activity of mitochondrial CIC.Transport of citrate into rat liver mitochondria that are freshly isolated (A) and into a reconstituted system (proteoliposomes) (B) was measured at the times indicated. The values reported in the figure represent the means ± SD (n = 4). *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
Mentions: The anabolic pathway of fatty acid synthesis utilizes the carbon units transported outside liver mitochondria by the CIC [19]. For this reason, we investigated the transport activity of this protein in freshly isolated mitochondria from liver of the three groups of rats. The transport activity of this mitochondrial carrier remained almost unaffected over time in the control group (Fig. 2A). Approximately the same trend was observed in the case of the HF group, i.e. almost no influence of the HF diet on the CIC activity over time. A small yet significant inhibition of the CIC activity in the HF group (about 12%) was only found after 4 weeks of dietary treatment (Fig. 2A). A net and significant decrease in the CIC activity was instead found in mitochondria isolated from the HF+KO group. After 12 weeks, such a decrease was 59% in the HF+KO group with respect to both control and HF groups. In this context, it is important to underline that the CIC protein operates in the inner mitochondrial membrane where it is deeply embedded. Therefore, its transport activity can be influenced, at least in principle, by the phospholipid and fatty acid composition of the inner mitochondrial membrane. In order to investigate this possibility, we extracted the CIC protein from the mitochondrial membranes using a non-denaturing detergent and subsequently purified it by hydroxyapatite chromatography. Eventually, the purified CIC was functionally reconstituted into liposomes, thereby obtaining the so-called proteoliposomes. The transport activity of the purified and reconstituted CIC from the HF+KO animals was significantly lower over time in comparison to that of both control and HF groups (Fig. 2B). An inhibition of about 60% was found at the 12th week of dietary treatment in HF+KO animals with respect to the other two groups of animals. Interestingly, the activity of the mitochondrial CIC in the rats of the HF group, excluding the inhibition observed after 4 weeks, was practically identical to that of the control rats (Fig. 2B). These observations imply that the addition of 2.5% KO to the HF diet (35% fat) is able to significantly decrease the transport activity of the mitochondrial CIC.

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