Regulatory effects of dietary n-3 and n-6 lipids on plasma and hepatic lipid levels, liver cell number and microsomal protein content in spontaneously hypertensive rats

Chen, H.W.; Lii, Chong‐Kuei; Ko, J.J.; Wang, S.T.; Hsu, Jeng-Dong

doi:10.1016/s0952-3278(96)90039-3

Cited by 14 publications

(7 citation statements)

References 61 publications

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“…Dietary 22:6n-3 has been associated with decreased 20:4n-6 in various tissues (19)(20)(21)(22)(23)(24)(25)(26), and dietary 22:6n-3 is considered to compete directly with 20:4n-6. It has been suggested that feeding 22:5n-6 along with 22:6n-3 may maintain 20:4n-6 levels in tissues via 22:5n-6 retroconversion (19).…”

Section: Discussionmentioning

confidence: 99%

Artificial rearing with docosahexaenoic acid and n-6 docosapentaenoic acid alters rat tissue fatty acid composition

Lim

Salem

2007

Journal of Lipid Research

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Section: Discussionmentioning

confidence: 99%

Artificial rearing with docosahexaenoic acid and n-6 docosapentaenoic acid alters rat tissue fatty acid composition

Lim

Salem

2007

Journal of Lipid Research

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“…In addition, we have previously found that hepatic cholesterol was signifi cantly higher in hamsters fed n-6 PUFA with the atherogenic diet than in those fed n-3 PUFA with the atherogenic diet [1,2,7] . It was also found that rats fed on a fi sh oil diet had signifi cantly lower liver total lipid and triglyceride concentrations than rats fed on a corn oil diet [23] . Based on these fi ndings, we also decided to measure cholesterol and triglyceride concentrations of liver in hamsters and rats fed n-3 PUFA or n-6 PUFA with a cholesterol-free diet, or with a diet enriched with cholesterol.…”

Section: Introductionmentioning

confidence: 95%

A High-Cholesterol, n–3 Polyunsaturated Fatty Acid Diet Causes Different Responses in Rats and Hamsters

Lin

Lu²,

Huang³

et al. 2005

Ann Nutr Metab

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This study was designed to investigate the response to a high-cholesterol, n–3 polyunsaturated fatty acid (PUFA) or n–6 PUFA diet in rats and hamsters. Animals were fed n–3 or n–6 PUFA with a cholesterol-free diet, or with a diet enriched with cholesterol (0.5%, w/w) for 2 weeks. In rats and hamsters fed a cholesterol-free diet, plasma cholesterol, triglycerides and very-low-density lipoprotein (VLDL)-triglyceride levels in n–3 PUFA group were significantly lower than those in n–6 PUFA group. In contrast, when diets were supplemented with 0.5% cholesterol, the plasma cholesterol- and triglyceride-lowering effect of dietary n–3 PUFA disappeared. In hamsters fed with the atherogenic diet (0.5% dietary cholesterol) for 2 weeks, n–3 PUFA induced hypercholesterolemia more than n–6 PUFA, the increase being in the VLDL and low-density lipoprotein (LDL) fractions. Our data thus indicate that elevation of VLDL- and LDL-cholesterol in hamsters by n–3 PUFA, compared with n–6 PUFA, is dependent on 0.5% dietary cholesterol supplementation. In rats, on the other hand, dietary n–3 PUFA did not induce hypercholesterolemia more than n–6 PUFA when 0.5% cholesterol was supplemented. Although the effects of n–3 PUFA on plasma cholesterol, triglycerides and VLDL-triglycerides were similar in hamsters and rats, the interactive effects of n–3 PUFA and cholesterol on plasma and lipoprotein cholesterol levels differed in the two species. It was also found that plasma triglycerides, cholesterol and lipoprotein cholesterol levels in hamsters are higher than in rats in the presence and absence of dietary cholesterol. In addition, cholesterol feeding induces hypertriglyceridemia and hypercholesterolemia only in hamsters. Moreover, liver triglyceride concentrations increased in rats fed a cholesterol-rich diet and hepatic triglyceride levels of the n–3 PUFA-fed rats were significantly lower than those in the n–6 PUFA-fed rats in the presence and absence of dietary cholesterol. However, triglycerides did not accumulate in the liver in hamsters fed a cholesterol-rich diet and hepatic triglyceride levels of the n–3 PUFA-fed hamsters were not significantly different from those in the n–6 PUFA-fed hamsters in the presence and absence of dietary cholesterol. Therefore, these studies confirm marked species differences in response to the interactive effects of dietary n–3 PUFA and cholesterol.

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“…On the other hand, in addition to 12-HETE, 2 pro-inflammation-related metabolites, 15-HETE (Calder, 2009) and 12-HEPE (Pilkington et al, 2014;Strassburg et al, 2012), were higher in the ND mice in comparison to the vehicle-treated ND mice. Moreover, the omega-3 polyunsaturated fatty acid eicosapentaenoate and the omega-6 polyunsaturated fatty acids, linoleate and arachidonate (Chen et al, 1996), were significantly lower and the ratio of omega-3/ omega-6 polyunsaturated fatty acids was apparently lower only in the ND mice at 24 hr. It was previously reported that a decrease in the ratio of omega-3/omega-6 polyunsaturated fatty acids may be a marker of pro-inflammation because omega-3 and omega-6 polyunsaturated fatty acids induce and reduce inflammation, respectively (Elabdeen et al, 2013;Kalogeropoulos et al, 2010).…”

Section: Discussionmentioning

confidence: 89%

Decreased hepatic phosphorylated p38 mitogen-activated protein kinase contributes to attenuation of thioacetamide-induced hepatic necrosis in diet-induced obese mice

et al. 2016

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-We previously reported that thioacetamide (TA)-induced hepatocellular necrosis was attenuated in mice fed a high-fat diet (HFD mice) compared with mice fed a normal rodent diet (ND mice). In this study, we investigated whether p38 mitogen-activated protein kinase (p38 MAPK) was involved in this attenuation. Western blot analysis revealed that hepatic phosphorylated p38 MAPK protein decreased at 8 and 24 hours (hr) after TA dosing in the HFD mice, while it decreased only at 24 hr in the ND mice in comparison to the time-and diet-matched, vehicle-treated mice. p38 MAPK regulates various biological functions including inflammation, therefore, hepatic metabolomics analysis focusing on pro-inflammatory lipid mediators was performed. At 24 hr after TA dosing, only one pro-inflammatory mediator, 12-hydroxyeicosatetraenoic acid (HETE), was higher in the HFD mice. On the other hand, in addition to 12-HETE, 15-HETE and 12-hydroxyeicosapentaenoic acid (HEPE) were higher and omega-3/ omega-6 polyunsaturated fatty acids ratios were lower in the ND mice at 24 hr. These results of metabolomics indicated that less pro-inflammatory state was seen in HFD mice than in ND mice at 24 hr. Finally, to confirm whether the observed decrease in phosphorylated p38 MAPK could attenuate TA-induced hepatocellular necrosis, we showed that SB203580 hydrochloride, an inhibitor of p38 MAPK, partially attenuated TA-induced hepatic necrosis in ND mice. Collectively, these results suggest that a prompt decrease in phosphorylation of p38 MAPK after TA administration is one of the factors that attenuate TAinduced hepatic necrosis in HFD mice.

show abstract

Regulatory effects of dietary n-3 and n-6 lipids on plasma and hepatic lipid levels, liver cell number and microsomal protein content in spontaneously hypertensive rats

Cited by 14 publications

References 61 publications

Artificial rearing with docosahexaenoic acid and n-6 docosapentaenoic acid alters rat tissue fatty acid composition

Artificial rearing with docosahexaenoic acid and n-6 docosapentaenoic acid alters rat tissue fatty acid composition

A High-Cholesterol, n–3 Polyunsaturated Fatty Acid Diet Causes Different Responses in Rats and Hamsters

Decreased hepatic phosphorylated p38 mitogen-activated protein kinase contributes to attenuation of thioacetamide-induced hepatic necrosis in diet-induced obese mice

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