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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 lipogenic enzyme activities.The activities of ACC (A) and FAS (B) were measured in the cytosol of rat hepatocytes at the times indicated. The values are expressed as nanomoles of NADH (ACC) or NADPH (FAS) oxidized min−1 mg protein−1 and 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-g004: Effect of KO on lipogenic enzyme activities.The activities of ACC (A) and FAS (B) were measured in the cytosol of rat hepatocytes at the times indicated. The values are expressed as nanomoles of NADH (ACC) or NADPH (FAS) oxidized min−1 mg protein−1 and represent the means ± SD (n = 4). *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.

Mentions: The activities of two cytosolic enzymes, ACC and FAS, to which the mitochondrial CIC supplies carbon units for hepatic fatty acid synthesis, were also investigated. A net decrease of the ACC activity in the HF+KO group was observed, when compared to that of both HF and control groups (Fig. 4A). After 12 weeks, the ACC activity in the HF+KO group was reduced by about 65%, when compared to control animals. A similar behaviour was observed in the case of the FAS activity (Fig. 4B), with approximately 60% inhibition in the HF+KO group. Hence, parallel inhibitions were found in the activities of the cytosolic ACC and FAS and 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 lipogenic enzyme activities.The activities of ACC (A) and FAS (B) were measured in the cytosol of rat hepatocytes at the times indicated. The values are expressed as nanomoles of NADH (ACC) or NADPH (FAS) oxidized min−1 mg protein−1 and 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-g004: Effect of KO on lipogenic enzyme activities.The activities of ACC (A) and FAS (B) were measured in the cytosol of rat hepatocytes at the times indicated. The values are expressed as nanomoles of NADH (ACC) or NADPH (FAS) oxidized min−1 mg protein−1 and represent the means ± SD (n = 4). *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
Mentions: The activities of two cytosolic enzymes, ACC and FAS, to which the mitochondrial CIC supplies carbon units for hepatic fatty acid synthesis, were also investigated. A net decrease of the ACC activity in the HF+KO group was observed, when compared to that of both HF and control groups (Fig. 4A). After 12 weeks, the ACC activity in the HF+KO group was reduced by about 65%, when compared to control animals. A similar behaviour was observed in the case of the FAS activity (Fig. 4B), with approximately 60% inhibition in the HF+KO group. Hence, parallel inhibitions were found in the activities of the cytosolic ACC and FAS and 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