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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 hepatic fatty acid oxidation.(A) CPT I activity was measured in liver mitochondria freshly isolated from rats at the times indicated. The values are expressed as nanomoles of DTNB reduced min−1·mg protein−1 and were calculated as described in the Methods section. (B) Liver carnitine levels were also determined at the times indicated. Data are 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-g005: Effect of KO on hepatic fatty acid oxidation.(A) CPT I activity was measured in liver mitochondria freshly isolated from rats at the times indicated. The values are expressed as nanomoles of DTNB reduced min−1·mg protein−1 and were calculated as described in the Methods section. (B) Liver carnitine levels were also determined at the times indicated. Data are means ± SD (n = 4). *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.

Mentions: The catabolic pathway of fatty acid oxidation occurs inside mitochondria and, from a metabolic point of view, represents the opposite of fatty acid synthesis. The rate-limiting step of fatty acid oxidation is represented by the activity of CPT I which is involved in the transport of fatty acids into the mitochondrial matrix. The activity of CPT I remained practically constant over time in the control rats (Fig. 5A). However, in the HF animals a clear decrease in the CPT I activity was detected at any time during the dietary treatment. The maximum degree of inhibition (51%) was seen after 8 weeks of dietary tratment. On the contrary, a significant increase in CPT I activity was found in the HF+KO rats. After 12 weeks of feeding, the CPT I activity was 2.1 and 3.4 fold higher than those of control and HF rats, respectively. Notably, these results were substantiated by the levels of hepatic carnitine detected in the three groups of animals (Fig. 5B). Carnitine is coupled to fatty acids in order to facilitate their passage across the inner mitochondrial membrane. In fact, the carnitine levels paralleled the trend of CPT I activities found in control, HF and HF+KO rats (Fig. 5B). This is in line with the fact that an increase (or a decrease) in CPT I activity is accompanied by parallel changes in free carnitine levels [25]. Thus, KO supplemented to the HF diet strongly stimulates fatty acid oxidation.


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 hepatic fatty acid oxidation.(A) CPT I activity was measured in liver mitochondria freshly isolated from rats at the times indicated. The values are expressed as nanomoles of DTNB reduced min−1·mg protein−1 and were calculated as described in the Methods section. (B) Liver carnitine levels were also determined at the times indicated. Data are 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-g005: Effect of KO on hepatic fatty acid oxidation.(A) CPT I activity was measured in liver mitochondria freshly isolated from rats at the times indicated. The values are expressed as nanomoles of DTNB reduced min−1·mg protein−1 and were calculated as described in the Methods section. (B) Liver carnitine levels were also determined at the times indicated. Data are means ± SD (n = 4). *P<0.05 vs. rats fed control diet; #P<0.05 vs. rats fed HF diet.
Mentions: The catabolic pathway of fatty acid oxidation occurs inside mitochondria and, from a metabolic point of view, represents the opposite of fatty acid synthesis. The rate-limiting step of fatty acid oxidation is represented by the activity of CPT I which is involved in the transport of fatty acids into the mitochondrial matrix. The activity of CPT I remained practically constant over time in the control rats (Fig. 5A). However, in the HF animals a clear decrease in the CPT I activity was detected at any time during the dietary treatment. The maximum degree of inhibition (51%) was seen after 8 weeks of dietary tratment. On the contrary, a significant increase in CPT I activity was found in the HF+KO rats. After 12 weeks of feeding, the CPT I activity was 2.1 and 3.4 fold higher than those of control and HF rats, respectively. Notably, these results were substantiated by the levels of hepatic carnitine detected in the three groups of animals (Fig. 5B). Carnitine is coupled to fatty acids in order to facilitate their passage across the inner mitochondrial membrane. In fact, the carnitine levels paralleled the trend of CPT I activities found in control, HF and HF+KO rats (Fig. 5B). This is in line with the fact that an increase (or a decrease) in CPT I activity is accompanied by parallel changes in free carnitine levels [25]. Thus, KO supplemented to the HF diet strongly stimulates fatty acid oxidation.

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