The Experts below are selected from a list of 192 Experts worldwide ranked by ideXlab platform
Rolf K. Berge - One of the best experts on this subject based on the ideXlab platform.
-
Hepatic steatosis induced in C57BL/6 mice by a non-ß oxidizable fatty acid analogue is associated with reduced plasma kynurenine metabolites and a modified hepatic NAD^+/NADH ratio
Lipids in Health and Disease, 2020Co-Authors: Rolf K. Berge, Jan E. Nordrehaug, Jon Skorve, Daniel Cacabelos, Rosa Señarís, Ottar Nygård, Bodil BjørndalAbstract:Background Non-alcoholic fatty liver disease is often associated with obesity, insulin resistance, dyslipidemia, and the metabolic syndrome in addition to mitochondrial dysfunction and nicotinamide adenine dinucleotide (NAD^+) deficiency. The aim of this study was to investigate how inhibition of mitochondrial fatty acid oxidation using the compound tetradecylthiopropionic acid (TTP) would affect hepatic Triacylglycerol Level and plasma Levels of kynurenine (Kyn) metabolites and nicotinamide. Methods 12 C57BL/6 mice were fed a control diet, or an intervention diet supplemented with 0.9% (w/w) tetradecylthiopropionic acid for 14 days. Blood and liver samples were collected, enzyme activities and gene expression were analyzed in liver, in addition to fatty acid composition. Metabolites in the tryptophan/kynurenine pathway and total antioxidant status were measured in plasma. Results Dietary treatment with tetradecylthiopropionic acid for 2 weeks induced fatty liver accompanied by decreased mitochondrial fatty acid oxidation. The liver content of the oxidized form of NAD^+ was increased, as well as the ratio of NAD^+/NADH, and these changes were associated by increased hepatic mRNA Levels of NAD synthetase and nicotinamide mononucleotide adenyltransferase-3. The downstream metabolites of kynurenine were reduced in plasma whereas the plasma nicotinamide content was increased. Some effects on inflammation and oxidative stress was observed in the liver, while the plasma antioxidant capacity was increased. This was accompanied by a reduced plasma ratio of kynurenine/tryptophan. In addition, a significant decrease in the inflammation-related arachidonic fatty acid in liver was observed. Conclusion Fatty liver induced by short-time treatment with tetradecylthiopropionic acid decreased the Levels of kynurenine metabolites but increased the plasma Levels of NAD^+ and nicotinamide. These changes are most likely not associated with increased inflammation and oxidative stress. Most probably the increase of NAD^+ and nicotinamide are generated through the Preiss Handler pathway and/or salvage pathway and not through the de novo pathway. The take home message is that non-alcoholic fatty liver disease is associated with the metabolic syndrome in addition to mitochondrial dysfunction and nicotinamide adenine dinucleotide (NAD^+) deficiency. Inducing fatty liver in mice by inhibition of fatty acid oxidation resulted in a concomitant change in kynurenine metabolites increasing the plasma Levels of nicotinamides and the hepatic NAD^+/NADH ratio, probably without affecting the de novo pathway of kynurenines.
-
Krill oil reduces plasma Triacylglycerol Level and improves related lipoprotein particle concentration, fatty acid composition and redox status in healthy young adults - a pilot study
Lipids in Health and Disease, 2015Co-Authors: Rolf K. Berge, Marie S. Ramsvik, Pavol Bohov, Asbjørn Svardal, Jan E. Nordrehaug, Espen Rostrup, Inge Bruheim, Bodil BjørndalAbstract:Background Lipid abnormalities, enhanced inflammation and oxidative stress seem to represent a vicious circle in atherogenesis, and therapeutic options directed against these processes seems like a reasonable approach in the management of atherosclerotic disorders. Krill oil (RIMFROST Sublime®) is a phospholipid-rich oil with eicosapentaenoic acid (EPA): docosahexaenoic acid (DHA) ratio of 1.8:1. In this pilot study we determined if krill oil could favourable affect plasma lipid parameters and parameters involved in the initiation and progression of atherosclerosis. Methods The study was conducted as a 28 days intervention study examining effect-parameters of dietary supplementation with krill oil (832.5 mg EPA and DHA per day). 17 healthy volunteers in the age group 18–36 (mean age 23 ± 4 years) participated. Plasma lipids, lipoprotein particle sizes, fatty acid composition in plasma and red blood cells (RBCs), plasma cytokines, antioxidant capacity, acylcarntines, carnitine, choline, betaine, and trimethylamine-N-oxide (TMAO) were measured before and after supplementation. Results Plasma Triacylglycerol (TAG) and large very-low density lipoprotein (VLDL) & chylomicron particle concentrations decreased after 28 days of krill oil intake. A significant reduction in the TAG/HDL cholesterol resulted. Krill oil supplementation decreased n-6/n-3 polyunsaturated fatty acids (PUFA) ratio both in plasma and RBCs. This was due to increased EPA, DHA and docosapentaenoic acid (DPA) and reduced amount of arachidonic acid (AA). The increase of n-3 fatty acids and wt % of EPA and DHA in RBC was of smaller magnitude than found in plasma. Krill oil intake increased the antioxidant capacity, double bond index (DBI) and the fatty acid anti-inflammatory index. The plasma atherogenicity index remained constant whereas the thrombogenicity index decreased. Plasma choline, betaine and the carnitine precursor, γ-butyrobetaine were increased after krill oil supplementation whereas the TMAO and carnitine concentrations remained unchanged. Conclusion Krill oil consumption is considered health beneficial as it decreases cardiovascular disease risk parameters through effects on plasma TAGs, lipoprotein particles, fatty acid profile, redox status and possible inflammation. Noteworthy, no adverse effects on plasma Levels of TMAO and carnitine were found.
-
krill oil reduces plasma Triacylglycerol Level and improves related lipoprotein particle concentration fatty acid composition and redox status in healthy young adults a pilot study
Lipids in Health and Disease, 2015Co-Authors: Rolf K. Berge, Marie S. Ramsvik, Pavol Bohov, Asbjørn Svardal, Jan E. Nordrehaug, Espen Rostrup, Inge Bruheim, Bodil BjørndalAbstract:Background Lipid abnormalities, enhanced inflammation and oxidative stress seem to represent a vicious circle in atherogenesis, and therapeutic options directed against these processes seems like a reasonable approach in the management of atherosclerotic disorders. Krill oil (RIMFROST Sublime®) is a phospholipid-rich oil with eicosapentaenoic acid (EPA): docosahexaenoic acid (DHA) ratio of 1.8:1. In this pilot study we determined if krill oil could favourable affect plasma lipid parameters and parameters involved in the initiation and progression of atherosclerosis.
-
krill protein hydrolysate reduces plasma Triacylglycerol Level with concurrent increase in plasma bile acid Level and hepatic fatty acid catabolism in high fat fed mice
Functional Foods in Health and Disease, 2013Co-Authors: Marie S. Ramsvik, Inge Bruheim, Bodil Bjørndal, Rita Vik, Jon Skorve, Rolf K. BergeAbstract:Background : Krill powder, consisting of both lipids and proteins, has been reported to modulate hepatic lipid catabolism in animals. Fish protein hydrolysate diets have also been reported to affect lipid metabolism and to elevate bile acid (BA) Level in plasma. BA interacts with a number of nuclear receptors and thus affects a variety of signaling pathways, including very low density lipoprotein (VLDL) secretion. The aim of the present study was to investigate whether a krill protein hydrolysate (KPH) could affect lipid and BA metabolism in mice. Method : C57BL/6 mice were fed a high-fat (21%, w/w) diet containing 20% crude protein (w/w) as casein (control group) or KPH for 6 weeks. Lipids and fatty acid composition were measured from plasma, enzyme activity and gene expression were analyzed from liver samples, and BA was measured from plasma. Results : The effect of dietary treatment with KPH resulted in reduced Levels of plasma Triacylglycerols (TAG) and non-esterified fatty acids (NEFAs). The KPH treated mice had also a marked increased plasma BA concentration. The increased plasma BA Level was associated with induction of genes related to membrane canalicular exporter proteins (Abcc2, Abcb4) and to BA exporters to blood (Abcc3 and Abcc4). Of note, we observed a 2-fold increased nuclear farnesoid X receptor (Fxr) mRNA Levels in the liver of mice fed KPH. We also observed increased activity of the nuclear peroxiosme proliferator-activated receptor alpha (PPARα) target gene carnitine plamitoyltransferase 2 (CPT-2). Conclusion : The KPH diet showed to influence lipid and BA metabolism in high-fat fed mice. Moreover, increased mitochondrial fatty acid oxidation and elevation of BA concentration may regulate the plasma Level of TAGs and NEFAs. Key words : Krill protein hydrolysate, Triacylglycerol, fatty acids, TNFα
-
Causes and prevention of tamoxifen-induced accumulation of Triacylglycerol in rat liver.
Journal of lipid research, 2006Co-Authors: Oddrun Anita Gudbrandsen, Therese H. Røst, Rolf K. BergeAbstract:Tamoxifen can induce hepatic steatosis in women. In this study, we wanted to elucidate the mechanism behind the tamoxifen-induced accumulation of Triacylglycerol in liver in female rats, and we hoped to prevent this development by combination treatment with the modified fatty acid tetradecylthioacetic acid (TTA). The increased hepatic Triacylglycerol Level after tamoxifen treatment was accompanied by decreased acetyl-coenzyme A carboxylase (ACC) and FAS activities, increased glycerol-3-phosphate acyltransferase (GPAT) activity, and a tendency to increased diacylglycerol acyltransferase (DGAT) activity. The activities and mRNA Levels of enzymes involved in β-oxidation, ketogenesis, and uptake of lipids from liver were unaffected by tamoxifen, whereas the uptake of lipoproteins was unchanged and the uptake of fatty acids was decreased. Combination treatment with tamoxifen and TTA (Tam+TTA) normalized the hepatic Triacylglycerol Level and increased the activities of ACC, FAS, GPAT, and DGAT compared with tamoxifen-treated rats. The activities and mRNA Levels of enzymes involved in β-oxidation, ketogenesis, and uptake of lipids were increased after Tam+TTA treatment. In conclusion, tamoxifen increased the hepatic Triacylglycerol Level, probably as a result of increased Triacylglycerol biosynthesis combined with unchanged β-oxidation. The tamoxifen-induced accumulation of Triacylglycerol was prevented by cotreatment with TTA, through mechanisms of increased mitochondrial and peroxisomal β-oxidation.
Bodil Bjørndal - One of the best experts on this subject based on the ideXlab platform.
-
Hepatic steatosis induced in C57BL/6 mice by a non-ß oxidizable fatty acid analogue is associated with reduced plasma kynurenine metabolites and a modified hepatic NAD^+/NADH ratio
Lipids in Health and Disease, 2020Co-Authors: Rolf K. Berge, Jan E. Nordrehaug, Jon Skorve, Daniel Cacabelos, Rosa Señarís, Ottar Nygård, Bodil BjørndalAbstract:Background Non-alcoholic fatty liver disease is often associated with obesity, insulin resistance, dyslipidemia, and the metabolic syndrome in addition to mitochondrial dysfunction and nicotinamide adenine dinucleotide (NAD^+) deficiency. The aim of this study was to investigate how inhibition of mitochondrial fatty acid oxidation using the compound tetradecylthiopropionic acid (TTP) would affect hepatic Triacylglycerol Level and plasma Levels of kynurenine (Kyn) metabolites and nicotinamide. Methods 12 C57BL/6 mice were fed a control diet, or an intervention diet supplemented with 0.9% (w/w) tetradecylthiopropionic acid for 14 days. Blood and liver samples were collected, enzyme activities and gene expression were analyzed in liver, in addition to fatty acid composition. Metabolites in the tryptophan/kynurenine pathway and total antioxidant status were measured in plasma. Results Dietary treatment with tetradecylthiopropionic acid for 2 weeks induced fatty liver accompanied by decreased mitochondrial fatty acid oxidation. The liver content of the oxidized form of NAD^+ was increased, as well as the ratio of NAD^+/NADH, and these changes were associated by increased hepatic mRNA Levels of NAD synthetase and nicotinamide mononucleotide adenyltransferase-3. The downstream metabolites of kynurenine were reduced in plasma whereas the plasma nicotinamide content was increased. Some effects on inflammation and oxidative stress was observed in the liver, while the plasma antioxidant capacity was increased. This was accompanied by a reduced plasma ratio of kynurenine/tryptophan. In addition, a significant decrease in the inflammation-related arachidonic fatty acid in liver was observed. Conclusion Fatty liver induced by short-time treatment with tetradecylthiopropionic acid decreased the Levels of kynurenine metabolites but increased the plasma Levels of NAD^+ and nicotinamide. These changes are most likely not associated with increased inflammation and oxidative stress. Most probably the increase of NAD^+ and nicotinamide are generated through the Preiss Handler pathway and/or salvage pathway and not through the de novo pathway. The take home message is that non-alcoholic fatty liver disease is associated with the metabolic syndrome in addition to mitochondrial dysfunction and nicotinamide adenine dinucleotide (NAD^+) deficiency. Inducing fatty liver in mice by inhibition of fatty acid oxidation resulted in a concomitant change in kynurenine metabolites increasing the plasma Levels of nicotinamides and the hepatic NAD^+/NADH ratio, probably without affecting the de novo pathway of kynurenines.
-
Krill oil reduces plasma Triacylglycerol Level and improves related lipoprotein particle concentration, fatty acid composition and redox status in healthy young adults - a pilot study
Lipids in Health and Disease, 2015Co-Authors: Rolf K. Berge, Marie S. Ramsvik, Pavol Bohov, Asbjørn Svardal, Jan E. Nordrehaug, Espen Rostrup, Inge Bruheim, Bodil BjørndalAbstract:Background Lipid abnormalities, enhanced inflammation and oxidative stress seem to represent a vicious circle in atherogenesis, and therapeutic options directed against these processes seems like a reasonable approach in the management of atherosclerotic disorders. Krill oil (RIMFROST Sublime®) is a phospholipid-rich oil with eicosapentaenoic acid (EPA): docosahexaenoic acid (DHA) ratio of 1.8:1. In this pilot study we determined if krill oil could favourable affect plasma lipid parameters and parameters involved in the initiation and progression of atherosclerosis. Methods The study was conducted as a 28 days intervention study examining effect-parameters of dietary supplementation with krill oil (832.5 mg EPA and DHA per day). 17 healthy volunteers in the age group 18–36 (mean age 23 ± 4 years) participated. Plasma lipids, lipoprotein particle sizes, fatty acid composition in plasma and red blood cells (RBCs), plasma cytokines, antioxidant capacity, acylcarntines, carnitine, choline, betaine, and trimethylamine-N-oxide (TMAO) were measured before and after supplementation. Results Plasma Triacylglycerol (TAG) and large very-low density lipoprotein (VLDL) & chylomicron particle concentrations decreased after 28 days of krill oil intake. A significant reduction in the TAG/HDL cholesterol resulted. Krill oil supplementation decreased n-6/n-3 polyunsaturated fatty acids (PUFA) ratio both in plasma and RBCs. This was due to increased EPA, DHA and docosapentaenoic acid (DPA) and reduced amount of arachidonic acid (AA). The increase of n-3 fatty acids and wt % of EPA and DHA in RBC was of smaller magnitude than found in plasma. Krill oil intake increased the antioxidant capacity, double bond index (DBI) and the fatty acid anti-inflammatory index. The plasma atherogenicity index remained constant whereas the thrombogenicity index decreased. Plasma choline, betaine and the carnitine precursor, γ-butyrobetaine were increased after krill oil supplementation whereas the TMAO and carnitine concentrations remained unchanged. Conclusion Krill oil consumption is considered health beneficial as it decreases cardiovascular disease risk parameters through effects on plasma TAGs, lipoprotein particles, fatty acid profile, redox status and possible inflammation. Noteworthy, no adverse effects on plasma Levels of TMAO and carnitine were found.
-
krill oil reduces plasma Triacylglycerol Level and improves related lipoprotein particle concentration fatty acid composition and redox status in healthy young adults a pilot study
Lipids in Health and Disease, 2015Co-Authors: Rolf K. Berge, Marie S. Ramsvik, Pavol Bohov, Asbjørn Svardal, Jan E. Nordrehaug, Espen Rostrup, Inge Bruheim, Bodil BjørndalAbstract:Background Lipid abnormalities, enhanced inflammation and oxidative stress seem to represent a vicious circle in atherogenesis, and therapeutic options directed against these processes seems like a reasonable approach in the management of atherosclerotic disorders. Krill oil (RIMFROST Sublime®) is a phospholipid-rich oil with eicosapentaenoic acid (EPA): docosahexaenoic acid (DHA) ratio of 1.8:1. In this pilot study we determined if krill oil could favourable affect plasma lipid parameters and parameters involved in the initiation and progression of atherosclerosis.
-
krill protein hydrolysate reduces plasma Triacylglycerol Level with concurrent increase in plasma bile acid Level and hepatic fatty acid catabolism in high fat fed mice
Functional Foods in Health and Disease, 2013Co-Authors: Marie S. Ramsvik, Inge Bruheim, Bodil Bjørndal, Rita Vik, Jon Skorve, Rolf K. BergeAbstract:Background : Krill powder, consisting of both lipids and proteins, has been reported to modulate hepatic lipid catabolism in animals. Fish protein hydrolysate diets have also been reported to affect lipid metabolism and to elevate bile acid (BA) Level in plasma. BA interacts with a number of nuclear receptors and thus affects a variety of signaling pathways, including very low density lipoprotein (VLDL) secretion. The aim of the present study was to investigate whether a krill protein hydrolysate (KPH) could affect lipid and BA metabolism in mice. Method : C57BL/6 mice were fed a high-fat (21%, w/w) diet containing 20% crude protein (w/w) as casein (control group) or KPH for 6 weeks. Lipids and fatty acid composition were measured from plasma, enzyme activity and gene expression were analyzed from liver samples, and BA was measured from plasma. Results : The effect of dietary treatment with KPH resulted in reduced Levels of plasma Triacylglycerols (TAG) and non-esterified fatty acids (NEFAs). The KPH treated mice had also a marked increased plasma BA concentration. The increased plasma BA Level was associated with induction of genes related to membrane canalicular exporter proteins (Abcc2, Abcb4) and to BA exporters to blood (Abcc3 and Abcc4). Of note, we observed a 2-fold increased nuclear farnesoid X receptor (Fxr) mRNA Levels in the liver of mice fed KPH. We also observed increased activity of the nuclear peroxiosme proliferator-activated receptor alpha (PPARα) target gene carnitine plamitoyltransferase 2 (CPT-2). Conclusion : The KPH diet showed to influence lipid and BA metabolism in high-fat fed mice. Moreover, increased mitochondrial fatty acid oxidation and elevation of BA concentration may regulate the plasma Level of TAGs and NEFAs. Key words : Krill protein hydrolysate, Triacylglycerol, fatty acids, TNFα
Haymie Choi - One of the best experts on this subject based on the ideXlab platform.
-
Stimulation of acyl-CoA oxidase by α-linolenic acid-rich perilla oil lowers plasma Triacylglycerol Level in rats
Life sciences, 2005Co-Authors: Hye-kyeong Kim, Haymie ChoiAbstract:Abstract The effect of dietary polyunsaturated fatty acids (PUFA) on hepatic peroxisomal oxidation was investigated with respect to the postprandial Triacylglycerol Levels. Male Sprague–Dawley rats were fed semipurified diets containing either 1% (w/w) corn oil, or 10% each of beef tallow, corn oil, perilla oil, and fish oil for 4 weeks and 4 days. Hepatic and plasma Triacylglycerol Levels were reduced in rats fed fish and perilla oil diets compared with corn oil and beef tallow diets. The peroxisomal β-oxidation, catalase activity, and acyl-CoA oxidase (AOX) activity were markedly increased by fish oil feeding. To a lesser extent, perilla oil elevated AOX activity in a 4-day feeding although the effect gradually decreased in a 4-week feeding. Similarly, the mRNA Levels were increased in rats fed fish and perilla oils. AOX activity was negatively correlated with postprandial Triacylglycerol Levels. In addition, the stimulation of AOX was highly associated with the content of long chain n-3 PUFA such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in hepatic microsome. These effects were evident within 4 days of initiating feeding. Therefore, α-linolenic perilla oil exerts a similar effect to fish oil in stimulating hepatic activity and gene expression of AOX by enriching long chain n-3 PUFA in hepatic membrane fraction, which can partly account for the reduction of postprandial triglyceridemia.
-
suppression of hepatic fatty acid synthase by feeding α linolenic acid rich perilla oil lowers plasma Triacylglycerol Level in rats
Journal of Nutritional Biochemistry, 2004Co-Authors: Hye-kyeong Kim, Sungwon Choi, Haymie ChoiAbstract:Abstract This study was performed to determine the effects of dietary perilla oil, a n-3 α-linolenic acid (ALA) source, on hepatic lipogenesis as a possible mechanism of lowering Triacylglycerol (TG) Levels. Male Sprague-Dawley rats were trained for a 3-hour feeding protocol and fed one of five semipurified diets as follows: 1% (w/w) corn oil control diet, or one of four diets supplemented with 10% each of beef tallow, corn oil, perilla oil, and fish oil. Two separate experiments were performed to compare the effects of feeding periods, 4 weeks and 4 days. Hepatic and plasma TG Levels were decreased in rats fed perilla oil and fish oil diets, compared with corn oil and beef tallow diets. The activities of hepatic lipogenic enzymes such as fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase, and malic enzyme were suppressed in the fish oil, perilla oil, and corn oil–fed groups, and the effect was the most significant in the fish oil–fed group. Also, the activities of glycolytic enzymes, glucokinase, and L-pyruvate kinase showed the similar trend as that of lipogenic enzymes. The activity of FAS, the key regulatory enzyme in lipogenesis, was positively correlated with hepatic and plasma TG Levels and reduced significantly in the perilla oil–fed group compared with corn oil–fed group. In addition, the FAS activity was negatively correlated with the hepatic microsomal content of EPA and DHA. In conclusion, suppression of FAS plays a significant role in the hypolipidemic effects observed in rats fed ALA rich perilla oil and these effects were associated with the increase of hepatic microsomal EPA and DHA contents.
Hye-kyeong Kim - One of the best experts on this subject based on the ideXlab platform.
-
Stimulation of acyl-CoA oxidase by α-linolenic acid-rich perilla oil lowers plasma Triacylglycerol Level in rats
Life sciences, 2005Co-Authors: Hye-kyeong Kim, Haymie ChoiAbstract:Abstract The effect of dietary polyunsaturated fatty acids (PUFA) on hepatic peroxisomal oxidation was investigated with respect to the postprandial Triacylglycerol Levels. Male Sprague–Dawley rats were fed semipurified diets containing either 1% (w/w) corn oil, or 10% each of beef tallow, corn oil, perilla oil, and fish oil for 4 weeks and 4 days. Hepatic and plasma Triacylglycerol Levels were reduced in rats fed fish and perilla oil diets compared with corn oil and beef tallow diets. The peroxisomal β-oxidation, catalase activity, and acyl-CoA oxidase (AOX) activity were markedly increased by fish oil feeding. To a lesser extent, perilla oil elevated AOX activity in a 4-day feeding although the effect gradually decreased in a 4-week feeding. Similarly, the mRNA Levels were increased in rats fed fish and perilla oils. AOX activity was negatively correlated with postprandial Triacylglycerol Levels. In addition, the stimulation of AOX was highly associated with the content of long chain n-3 PUFA such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in hepatic microsome. These effects were evident within 4 days of initiating feeding. Therefore, α-linolenic perilla oil exerts a similar effect to fish oil in stimulating hepatic activity and gene expression of AOX by enriching long chain n-3 PUFA in hepatic membrane fraction, which can partly account for the reduction of postprandial triglyceridemia.
-
suppression of hepatic fatty acid synthase by feeding α linolenic acid rich perilla oil lowers plasma Triacylglycerol Level in rats
Journal of Nutritional Biochemistry, 2004Co-Authors: Hye-kyeong Kim, Sungwon Choi, Haymie ChoiAbstract:Abstract This study was performed to determine the effects of dietary perilla oil, a n-3 α-linolenic acid (ALA) source, on hepatic lipogenesis as a possible mechanism of lowering Triacylglycerol (TG) Levels. Male Sprague-Dawley rats were trained for a 3-hour feeding protocol and fed one of five semipurified diets as follows: 1% (w/w) corn oil control diet, or one of four diets supplemented with 10% each of beef tallow, corn oil, perilla oil, and fish oil. Two separate experiments were performed to compare the effects of feeding periods, 4 weeks and 4 days. Hepatic and plasma TG Levels were decreased in rats fed perilla oil and fish oil diets, compared with corn oil and beef tallow diets. The activities of hepatic lipogenic enzymes such as fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase, and malic enzyme were suppressed in the fish oil, perilla oil, and corn oil–fed groups, and the effect was the most significant in the fish oil–fed group. Also, the activities of glycolytic enzymes, glucokinase, and L-pyruvate kinase showed the similar trend as that of lipogenic enzymes. The activity of FAS, the key regulatory enzyme in lipogenesis, was positively correlated with hepatic and plasma TG Levels and reduced significantly in the perilla oil–fed group compared with corn oil–fed group. In addition, the FAS activity was negatively correlated with the hepatic microsomal content of EPA and DHA. In conclusion, suppression of FAS plays a significant role in the hypolipidemic effects observed in rats fed ALA rich perilla oil and these effects were associated with the increase of hepatic microsomal EPA and DHA contents.
Jan E. Nordrehaug - One of the best experts on this subject based on the ideXlab platform.
-
Hepatic steatosis induced in C57BL/6 mice by a non-ß oxidizable fatty acid analogue is associated with reduced plasma kynurenine metabolites and a modified hepatic NAD^+/NADH ratio
Lipids in Health and Disease, 2020Co-Authors: Rolf K. Berge, Jan E. Nordrehaug, Jon Skorve, Daniel Cacabelos, Rosa Señarís, Ottar Nygård, Bodil BjørndalAbstract:Background Non-alcoholic fatty liver disease is often associated with obesity, insulin resistance, dyslipidemia, and the metabolic syndrome in addition to mitochondrial dysfunction and nicotinamide adenine dinucleotide (NAD^+) deficiency. The aim of this study was to investigate how inhibition of mitochondrial fatty acid oxidation using the compound tetradecylthiopropionic acid (TTP) would affect hepatic Triacylglycerol Level and plasma Levels of kynurenine (Kyn) metabolites and nicotinamide. Methods 12 C57BL/6 mice were fed a control diet, or an intervention diet supplemented with 0.9% (w/w) tetradecylthiopropionic acid for 14 days. Blood and liver samples were collected, enzyme activities and gene expression were analyzed in liver, in addition to fatty acid composition. Metabolites in the tryptophan/kynurenine pathway and total antioxidant status were measured in plasma. Results Dietary treatment with tetradecylthiopropionic acid for 2 weeks induced fatty liver accompanied by decreased mitochondrial fatty acid oxidation. The liver content of the oxidized form of NAD^+ was increased, as well as the ratio of NAD^+/NADH, and these changes were associated by increased hepatic mRNA Levels of NAD synthetase and nicotinamide mononucleotide adenyltransferase-3. The downstream metabolites of kynurenine were reduced in plasma whereas the plasma nicotinamide content was increased. Some effects on inflammation and oxidative stress was observed in the liver, while the plasma antioxidant capacity was increased. This was accompanied by a reduced plasma ratio of kynurenine/tryptophan. In addition, a significant decrease in the inflammation-related arachidonic fatty acid in liver was observed. Conclusion Fatty liver induced by short-time treatment with tetradecylthiopropionic acid decreased the Levels of kynurenine metabolites but increased the plasma Levels of NAD^+ and nicotinamide. These changes are most likely not associated with increased inflammation and oxidative stress. Most probably the increase of NAD^+ and nicotinamide are generated through the Preiss Handler pathway and/or salvage pathway and not through the de novo pathway. The take home message is that non-alcoholic fatty liver disease is associated with the metabolic syndrome in addition to mitochondrial dysfunction and nicotinamide adenine dinucleotide (NAD^+) deficiency. Inducing fatty liver in mice by inhibition of fatty acid oxidation resulted in a concomitant change in kynurenine metabolites increasing the plasma Levels of nicotinamides and the hepatic NAD^+/NADH ratio, probably without affecting the de novo pathway of kynurenines.
-
Krill oil reduces plasma Triacylglycerol Level and improves related lipoprotein particle concentration, fatty acid composition and redox status in healthy young adults - a pilot study
Lipids in Health and Disease, 2015Co-Authors: Rolf K. Berge, Marie S. Ramsvik, Pavol Bohov, Asbjørn Svardal, Jan E. Nordrehaug, Espen Rostrup, Inge Bruheim, Bodil BjørndalAbstract:Background Lipid abnormalities, enhanced inflammation and oxidative stress seem to represent a vicious circle in atherogenesis, and therapeutic options directed against these processes seems like a reasonable approach in the management of atherosclerotic disorders. Krill oil (RIMFROST Sublime®) is a phospholipid-rich oil with eicosapentaenoic acid (EPA): docosahexaenoic acid (DHA) ratio of 1.8:1. In this pilot study we determined if krill oil could favourable affect plasma lipid parameters and parameters involved in the initiation and progression of atherosclerosis. Methods The study was conducted as a 28 days intervention study examining effect-parameters of dietary supplementation with krill oil (832.5 mg EPA and DHA per day). 17 healthy volunteers in the age group 18–36 (mean age 23 ± 4 years) participated. Plasma lipids, lipoprotein particle sizes, fatty acid composition in plasma and red blood cells (RBCs), plasma cytokines, antioxidant capacity, acylcarntines, carnitine, choline, betaine, and trimethylamine-N-oxide (TMAO) were measured before and after supplementation. Results Plasma Triacylglycerol (TAG) and large very-low density lipoprotein (VLDL) & chylomicron particle concentrations decreased after 28 days of krill oil intake. A significant reduction in the TAG/HDL cholesterol resulted. Krill oil supplementation decreased n-6/n-3 polyunsaturated fatty acids (PUFA) ratio both in plasma and RBCs. This was due to increased EPA, DHA and docosapentaenoic acid (DPA) and reduced amount of arachidonic acid (AA). The increase of n-3 fatty acids and wt % of EPA and DHA in RBC was of smaller magnitude than found in plasma. Krill oil intake increased the antioxidant capacity, double bond index (DBI) and the fatty acid anti-inflammatory index. The plasma atherogenicity index remained constant whereas the thrombogenicity index decreased. Plasma choline, betaine and the carnitine precursor, γ-butyrobetaine were increased after krill oil supplementation whereas the TMAO and carnitine concentrations remained unchanged. Conclusion Krill oil consumption is considered health beneficial as it decreases cardiovascular disease risk parameters through effects on plasma TAGs, lipoprotein particles, fatty acid profile, redox status and possible inflammation. Noteworthy, no adverse effects on plasma Levels of TMAO and carnitine were found.
-
krill oil reduces plasma Triacylglycerol Level and improves related lipoprotein particle concentration fatty acid composition and redox status in healthy young adults a pilot study
Lipids in Health and Disease, 2015Co-Authors: Rolf K. Berge, Marie S. Ramsvik, Pavol Bohov, Asbjørn Svardal, Jan E. Nordrehaug, Espen Rostrup, Inge Bruheim, Bodil BjørndalAbstract:Background Lipid abnormalities, enhanced inflammation and oxidative stress seem to represent a vicious circle in atherogenesis, and therapeutic options directed against these processes seems like a reasonable approach in the management of atherosclerotic disorders. Krill oil (RIMFROST Sublime®) is a phospholipid-rich oil with eicosapentaenoic acid (EPA): docosahexaenoic acid (DHA) ratio of 1.8:1. In this pilot study we determined if krill oil could favourable affect plasma lipid parameters and parameters involved in the initiation and progression of atherosclerosis.
