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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 respiratory complexes activity, expression, and function. Effect of KO on respiratory complexes activity (a). Enzymatic activities measured in the control group were set to 100%. Effect of KO on OXPHOS proteins levels (b). Liver mitochondrial proteins from control, HF, or HF+KO-fed rats were separated by SDS-PAGE, transferred to nitrocellulose, and then immunodecorated with a cocktail against NDUFB8, SDHB, COR2, COX1, ATP5A, or the mammalian porin as a control. The amount of OXPHOS proteins revealed by immunodecoration in the control group was set to 100% (c). ATP and LPO quantification of liver samples isolated from animals fed a control diet, a HF diet, or a HF+KO (d). The amount of ATP or LPO (expressed as nmoles per mg protein) 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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fig3: Effect of KO on respiratory complexes activity, expression, and function. Effect of KO on respiratory complexes activity (a). Enzymatic activities measured in the control group were set to 100%. Effect of KO on OXPHOS proteins levels (b). Liver mitochondrial proteins from control, HF, or HF+KO-fed rats were separated by SDS-PAGE, transferred to nitrocellulose, and then immunodecorated with a cocktail against NDUFB8, SDHB, COR2, COX1, ATP5A, or the mammalian porin as a control. The amount of OXPHOS proteins revealed by immunodecoration in the control group was set to 100% (c). ATP and LPO quantification of liver samples isolated from animals fed a control diet, a HF diet, or a HF+KO (d). The amount of ATP or LPO (expressed as nmoles per mg protein) 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: In a more selective approach for investigating the functionality of the mitochondrial oxidative phosphorylation we assayed the activity of single components of the respiratory chain: complexes I–IV and ATP-synthase (Figure 3(a)). A significant decrease (about 30%) in the activity of all respiratory chain complexes was found in HF animals. On the contrary, the values of complexes activity of the HF+KO rats were practically identical to those measured in control animals.


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 respiratory complexes activity, expression, and function. Effect of KO on respiratory complexes activity (a). Enzymatic activities measured in the control group were set to 100%. Effect of KO on OXPHOS proteins levels (b). Liver mitochondrial proteins from control, HF, or HF+KO-fed rats were separated by SDS-PAGE, transferred to nitrocellulose, and then immunodecorated with a cocktail against NDUFB8, SDHB, COR2, COX1, ATP5A, or the mammalian porin as a control. The amount of OXPHOS proteins revealed by immunodecoration in the control group was set to 100% (c). ATP and LPO quantification of liver samples isolated from animals fed a control diet, a HF diet, or a HF+KO (d). The amount of ATP or LPO (expressed as nmoles per mg protein) 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

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getmorefigures.php?uid=PMC4537729&req=5

fig3: Effect of KO on respiratory complexes activity, expression, and function. Effect of KO on respiratory complexes activity (a). Enzymatic activities measured in the control group were set to 100%. Effect of KO on OXPHOS proteins levels (b). Liver mitochondrial proteins from control, HF, or HF+KO-fed rats were separated by SDS-PAGE, transferred to nitrocellulose, and then immunodecorated with a cocktail against NDUFB8, SDHB, COR2, COX1, ATP5A, or the mammalian porin as a control. The amount of OXPHOS proteins revealed by immunodecoration in the control group was set to 100% (c). ATP and LPO quantification of liver samples isolated from animals fed a control diet, a HF diet, or a HF+KO (d). The amount of ATP or LPO (expressed as nmoles per mg protein) 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: In a more selective approach for investigating the functionality of the mitochondrial oxidative phosphorylation we assayed the activity of single components of the respiratory chain: complexes I–IV and ATP-synthase (Figure 3(a)). A significant decrease (about 30%) in the activity of all respiratory chain complexes was found in HF animals. On the contrary, the values of complexes activity of the HF+KO rats were practically identical to those measured in control animals.

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