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Krill Oil Ameliorates Mitochondrial Dysfunctions in Rats Treated with High-Fat Diet.

Ferramosca A, Conte A, Zara V - Biomed Res Int (2015)

Bottom Line: On the other hand, krill oil, a novel dietary supplement of n-3 PUFAs, has the ability to improve lipid and glucose metabolism, exerting possible protective effects against hepatic steatosis.This effect is obtained by stimulating mitochondrial metabolic pathways such as fatty acid oxidation, Krebs cycle, and respiratory chain complexes activity.Modulation of the expression of carrier proteins involved in mitochondrial uncoupling was also observed.

View Article: PubMed Central - PubMed

Affiliation: Dipartimento di Scienze e Tecnologie Biologiche ed Ambientali, Università del Salento, Via Provinciale Lecce-Monteroni, 73100 Lecce, Italy.

ABSTRACT
In recent years, several studies focused their attention on the role of dietary fats in the pathogenesis of hepatic steatosis. It has been demonstrated that a high-fat diet is able to induce hyperglycemia, hyperinsulinemia, obesity, and nonalcoholic fatty liver disease. On the other hand, krill oil, a novel dietary supplement of n-3 PUFAs, has the ability to improve lipid and glucose metabolism, exerting possible protective effects against hepatic steatosis. In this study we have investigated the effects of krill oil on mitochondrial energetic metabolism in animals fed a high-fat diet. To this end, male Sprague-Dawley rats were divided into three groups and fed for 4 weeks with a standard diet (control group), a diet with 35% fat (HF group), or a high-fat diet supplemented with 2.5% krill oil (HF+KO group). The obtained results suggest that krill oil promotes the burning of fat excess introduced by the high-fat diet. This effect is obtained by stimulating mitochondrial metabolic pathways such as fatty acid oxidation, Krebs cycle, and respiratory chain complexes activity. Modulation of the expression of carrier proteins involved in mitochondrial uncoupling was also observed. Overall, krill oil counteracts the negative effects of a high-fat diet on mitochondrial energetic metabolism.

No MeSH data available.


Related in: MedlinePlus

Effect of KO on proteins related to the respiratory chain function. Effect of KO on proteins levels of UCP2 (a) and AAC (b). The amount of porin, an outer membrane protein, was tested as a control (c). 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 UCP2, AAC or the mammalian porin. The amount of proteins revealed by immunodecoration in the control group was set to 100%. The values reported in the figure represent the means ± SD (n = 5). *P < 0.05 versus rats fed control diet; #P < 0.05 versus rats fed HF diet.
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fig4: Effect of KO on proteins related to the respiratory chain function. Effect of KO on proteins levels of UCP2 (a) and AAC (b). The amount of porin, an outer membrane protein, was tested as a control (c). 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 UCP2, AAC or the mammalian porin. The amount of proteins revealed by immunodecoration in the control group was set to 100%. The values reported in the figure represent the means ± SD (n = 5). *P < 0.05 versus rats fed control diet; #P < 0.05 versus rats fed HF diet.

Mentions: Uncoupling protein 2 (UCP2) uncouples respiration from oxidative phosphorylation. We therefore analyzed the expression profile of this carrier protein in the three groups of animals (Figure 4(a)). After 4 weeks of HF dietary treatment the amount of this protein increased about 5-fold, compared to the control group. Interestingly, a significant smaller increase in the expression of UCP2 was found after KO supplementation. In fact, in the presence of KO in the HF diet the level of this carrier protein was about 50% of that found in HF rats.


Krill Oil Ameliorates Mitochondrial Dysfunctions in Rats Treated with High-Fat Diet.

Ferramosca A, Conte A, Zara V - Biomed Res Int (2015)

Effect of KO on proteins related to the respiratory chain function. Effect of KO on proteins levels of UCP2 (a) and AAC (b). The amount of porin, an outer membrane protein, was tested as a control (c). 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 UCP2, AAC or the mammalian porin. The amount of proteins revealed by immunodecoration in the control group was set to 100%. The values reported in the figure represent the means ± SD (n = 5). *P < 0.05 versus rats fed control diet; #P < 0.05 versus rats fed HF diet.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4537729&req=5

fig4: Effect of KO on proteins related to the respiratory chain function. Effect of KO on proteins levels of UCP2 (a) and AAC (b). The amount of porin, an outer membrane protein, was tested as a control (c). 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 UCP2, AAC or the mammalian porin. The amount of proteins revealed by immunodecoration in the control group was set to 100%. The values reported in the figure represent the means ± SD (n = 5). *P < 0.05 versus rats fed control diet; #P < 0.05 versus rats fed HF diet.
Mentions: Uncoupling protein 2 (UCP2) uncouples respiration from oxidative phosphorylation. We therefore analyzed the expression profile of this carrier protein in the three groups of animals (Figure 4(a)). After 4 weeks of HF dietary treatment the amount of this protein increased about 5-fold, compared to the control group. Interestingly, a significant smaller increase in the expression of UCP2 was found after KO supplementation. In fact, in the presence of KO in the HF diet the level of this carrier protein was about 50% of that found in HF rats.

Bottom Line: On the other hand, krill oil, a novel dietary supplement of n-3 PUFAs, has the ability to improve lipid and glucose metabolism, exerting possible protective effects against hepatic steatosis.This effect is obtained by stimulating mitochondrial metabolic pathways such as fatty acid oxidation, Krebs cycle, and respiratory chain complexes activity.Modulation of the expression of carrier proteins involved in mitochondrial uncoupling was also observed.

View Article: PubMed Central - PubMed

Affiliation: Dipartimento di Scienze e Tecnologie Biologiche ed Ambientali, Università del Salento, Via Provinciale Lecce-Monteroni, 73100 Lecce, Italy.

ABSTRACT
In recent years, several studies focused their attention on the role of dietary fats in the pathogenesis of hepatic steatosis. It has been demonstrated that a high-fat diet is able to induce hyperglycemia, hyperinsulinemia, obesity, and nonalcoholic fatty liver disease. On the other hand, krill oil, a novel dietary supplement of n-3 PUFAs, has the ability to improve lipid and glucose metabolism, exerting possible protective effects against hepatic steatosis. In this study we have investigated the effects of krill oil on mitochondrial energetic metabolism in animals fed a high-fat diet. To this end, male Sprague-Dawley rats were divided into three groups and fed for 4 weeks with a standard diet (control group), a diet with 35% fat (HF group), or a high-fat diet supplemented with 2.5% krill oil (HF+KO group). The obtained results suggest that krill oil promotes the burning of fat excess introduced by the high-fat diet. This effect is obtained by stimulating mitochondrial metabolic pathways such as fatty acid oxidation, Krebs cycle, and respiratory chain complexes activity. Modulation of the expression of carrier proteins involved in mitochondrial uncoupling was also observed. Overall, krill oil counteracts the negative effects of a high-fat diet on mitochondrial energetic metabolism.

No MeSH data available.


Related in: MedlinePlus