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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 plasma levels of glucose and insulin.(A) Blood glucose concentrations were determined using reactive strips and a commercial glucometer. (B) Plasma insulin concentrations were analyzed with commercial enzyme-linked immunosorbent assay kits. 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-g011: Effect of KO on plasma levels of glucose and insulin.(A) Blood glucose concentrations were determined using reactive strips and a commercial glucometer. (B) Plasma insulin concentrations were analyzed with commercial enzyme-linked immunosorbent assay kits. 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 blood glucose concentration increased in both HF (76%) and HF+KO (72%) animals after 4 weeks of dietary administration, in comparison to control rats (Fig. 11A). From the 4th week onward, there was a progressive normalization in the levels of blood glucose in the HF+KO treated animals, which resulted in only slightly increased level after 12 weeks (13%), compared to control rats. On the contrary, the modifications in glucose level were more persistent in the HF treated animals, compared to the control group (+33% at the 12th week). A sudden and massive increase in the levels of insulin was revealed in the plasma of HF animals, in comparison to control rats (Fig. 11B). After 12 weeks of dietary treatment, insulin was increased 2.15 fold in HF animals, in comparison to the control ones. However, the concentration of plasma insulin in rats supplemented with KO was comparable to that of control animals at any time during the dietary treatment (Fig. 11B). KO is therefore able to efficiently counteract the hyperglycidemic effects of a HF diet by normalizing the blood glucose level and preventing an increase in the plasma insulin concentration.


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 plasma levels of glucose and insulin.(A) Blood glucose concentrations were determined using reactive strips and a commercial glucometer. (B) Plasma insulin concentrations were analyzed with commercial enzyme-linked immunosorbent assay kits. 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-g011: Effect of KO on plasma levels of glucose and insulin.(A) Blood glucose concentrations were determined using reactive strips and a commercial glucometer. (B) Plasma insulin concentrations were analyzed with commercial enzyme-linked immunosorbent assay kits. 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 blood glucose concentration increased in both HF (76%) and HF+KO (72%) animals after 4 weeks of dietary administration, in comparison to control rats (Fig. 11A). From the 4th week onward, there was a progressive normalization in the levels of blood glucose in the HF+KO treated animals, which resulted in only slightly increased level after 12 weeks (13%), compared to control rats. On the contrary, the modifications in glucose level were more persistent in the HF treated animals, compared to the control group (+33% at the 12th week). A sudden and massive increase in the levels of insulin was revealed in the plasma of HF animals, in comparison to control rats (Fig. 11B). After 12 weeks of dietary treatment, insulin was increased 2.15 fold in HF animals, in comparison to the control ones. However, the concentration of plasma insulin in rats supplemented with KO was comparable to that of control animals at any time during the dietary treatment (Fig. 11B). KO is therefore able to efficiently counteract the hyperglycidemic effects of a HF diet by normalizing the blood glucose level and preventing an increase in the plasma insulin concentration.

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