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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

Mitochondrial metabolic pathways from glucose and fatty acid oxidation. Schematic picture of the metabolic pathways from glucose and fatty acid oxidation (a). Effect of KO on the activity of mitochondrial enzymes PDH (b), CPT I (c), and CS (d) in control, HF, or HF+KO-fed rats liver. The values reported in the figure represent the means ± SD (n = 5). *P < 0.05 versus rats fed a control diet; #P < 0.05 versus rats fed a HF diet.
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fig2: Mitochondrial metabolic pathways from glucose and fatty acid oxidation. Schematic picture of the metabolic pathways from glucose and fatty acid oxidation (a). Effect of KO on the activity of mitochondrial enzymes PDH (b), CPT I (c), and CS (d) in control, HF, or HF+KO-fed rats liver. The values reported in the figure represent the means ± SD (n = 5). *P < 0.05 versus rats fed a control diet; #P < 0.05 versus rats fed a HF diet.

Mentions: Mitochondria play a central role in energy production. Sugars and fatty acids undergo glycolysis and mitochondrial β-oxidation, respectively, to produce acetyl-CoA (Figure 2(a)). PDH complex activity is the major determinant of glucose oxidation in animal cells. We found that PDH activity remained unchanged in the three groups of animals, suggesting that glucose catabolism was not affected by a HF diet or by KO supplementation (Figure 2(b)).


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

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

Mitochondrial metabolic pathways from glucose and fatty acid oxidation. Schematic picture of the metabolic pathways from glucose and fatty acid oxidation (a). Effect of KO on the activity of mitochondrial enzymes PDH (b), CPT I (c), and CS (d) in control, HF, or HF+KO-fed rats liver. The values reported in the figure represent the means ± SD (n = 5). *P < 0.05 versus rats fed a control diet; #P < 0.05 versus rats fed a HF diet.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig2: Mitochondrial metabolic pathways from glucose and fatty acid oxidation. Schematic picture of the metabolic pathways from glucose and fatty acid oxidation (a). Effect of KO on the activity of mitochondrial enzymes PDH (b), CPT I (c), and CS (d) in control, HF, or HF+KO-fed rats liver. The values reported in the figure represent the means ± SD (n = 5). *P < 0.05 versus rats fed a control diet; #P < 0.05 versus rats fed a HF diet.
Mentions: Mitochondria play a central role in energy production. Sugars and fatty acids undergo glycolysis and mitochondrial β-oxidation, respectively, to produce acetyl-CoA (Figure 2(a)). PDH complex activity is the major determinant of glucose oxidation in animal cells. We found that PDH activity remained unchanged in the three groups of animals, suggesting that glucose catabolism was not affected by a HF diet or by KO supplementation (Figure 2(b)).

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