Docosahexaenoic Acid and Arachidonic Acid Prevent Essential Fatty Acid Deficiency and Hepatic Steatosis

Le, Hau D.; Meisel, Jonathan A.; Meijer, Vincent E de; Fallon, Erica M.; Gura, Kathleen M.; Nosé, Vânia; Bistrian, Bruce R.; Puder, Mark

doi:10.1177/0148607111414580

Cited by 27 publications

(23 citation statements)

References 29 publications

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“…The activation of PPAR-γ was shown to have a relationship with expression of collagen type I induced by TGF-β1 (Bian et al, 2013) and inhibit hepatic stellate cell activation and progression of fibrosis (Attia et al, 2013). Studies have indicated that arachidonic acid is involved in oxidative stress and in inflammatory response (Holownia et al, 2014;Le et al, 2012;Xie et al, 2015) which was also been proved in our GO analysis. ALDH2 and ALDH7A1 were involved in glycolysis/Gluconeogenesis and glycerolipid metabolism, and the results of qRT-PCR and Western blot showed that the expression of ALDH2 and ALDH7A1 decreased after liver injury.…”

Section: Discussionsupporting

confidence: 70%

Mechanisms of CCl<sub>4</sub>-induced liver fibrosis with combined transcriptomic and proteomic analysis

et al. 2016

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-The classic toxicity of carbon tetrachloride (CCl 4 ) is to induce liver lesion and liver fibrosis. Liver fibrosis is a consequence of chronic liver lesion, which can progress into liver cirrhosis even hepatocarcinoma. However, the toxicological mechanisms of CCl 4 -induced liver fibrosis remain not fully understood. We combined transcriptomic and proteomic analysis and biological network technology, predicted toxicological targets and regulatory networks of CCl 4 in liver fibrosis. Wistar rats were treated with CCl 4 for 9 weeks. Histopathological changes, hydroxyproline (Hyp) contents, serum ALT and AST in the CCl 4 -treated group were significantly higher than that of CCl 4 -untreated group. CCl 4 -treated and -untreated liver tissues were examined by microarray and iTRAQ. The results showed that 3535 genes (fold change ≥ 1.5, P < 0.05) and 1412 proteins (fold change ≥ 1.2, P < 0.05) were differentially expressed. Moreover, the integrative analysis of transcriptomics and proteomics data showed 523 overlapped proteins, enriched in 182 GO terms including oxidation reduction, response to oxidative stress, inflammatory response, extracellular matrix organization, etc. Furthermore, KEGG pathway analysis showed that 36 pathways including retinol metabolism, PPAR signaling pathway, glycolysis/gluconeogenesis, arachidonic acid metabolism, metabolism of xenobiotics by cytochrome P450 and drug metabolism. Network of protein-protein interaction (PPI) and key function with their related targets were performed and the degree of network was calculated with Cytoscape. The expression of key targets such as CYP4A3, ALDH2 and ALDH7A1 decreased after CCl 4 treatment. Therefore, the toxicological mechanisms of CCl 4 -induced liver fibrosis may be related with multi biological process, pathway and targets which may provide potential protection reaction mechanism for CCl 4 detoxication in the liver.

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Section: Discussionsupporting

confidence: 70%

Mechanisms of CCl<sub>4</sub>-induced liver fibrosis with combined transcriptomic and proteomic analysis

et al. 2016

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“…An omega-3 FA rich diet (DHA) was designed to mimic the FA composition of cold water fish (21, 22), with an omega-3 to omega-6 FA ratio of 20:1 provided as DHA and arachidonic acid (AA; 20:4n-6; omega-6 FA). In contrast an omega-6 FA rich diet (SOY) was designed to mimic the standard western diet, with fat provided as soybean oil and thus containing an omega-6 to omega-3 FA ratio of ~8:1 provided as linoleic acid (LA; 18:2n-6; omega-6 FA) and alpha-linolenic acid (ALA; 18:3n-3; omega-3 FA).…”

Section: Resultsmentioning

confidence: 99%

Docosahexaenoic acid, G protein–coupled receptors, and melanoma: is G protein–coupled receptor 40 a potential therapeutic target?

Nehra¹,

Pan²,

Le³

et al. 2014

Journal of Surgical Research

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Purpose To determine the effect of docosahexaenoic acid (DHA) on the growth of human melanoma in vitro and in vivo and to better understand the potential role of the G-protein coupled receptors in mediating this effect. Materials and Methods For in vitro studies, human melanoma and control fibroblast cells were treated with DHA and TAK-875 (selective GPR40 agonist) and a cell viability assay was performed to determine cell counts. A murine subcutaneous xenograft model of human melanoma was used to test the effect of dietary treatment with an omega-3 fatty acid (FA) rich diet compared to an omega-6 FA rich diet on the growth of human melanoma in vivo. A similar animal model was used to test the effect of oral TAK-875 on the growth of established melanoma tumors in vivo. Results DHA has an inhibitory effect on the growth of human melanoma both in vitro and in vivo. Tumors from animals on the omega-3 FA rich diet were 69% smaller in weight (P=0.005) and 76% smaller in volume compared to tumors from animals on the omega-6 FA rich diet. TAK-875 has an inhibitory effect on the growth of human melanoma both in vitro and in vivo. Tumors from animals treated with TAK-875 were 46% smaller in weight (P=0.07), 62% smaller in volume (P=0.03) and grew 77% slower (P=0.04) compared to the placebo group. Conclusion DHA and TAK-875 have a profound and selective inhibitory effect on the growth of human melanoma both in vitro and in vivo.

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“…To this end, an omega-3 fatty acid-rich diet was designed to mimic the fatty acid composition of cold water fish (Le et al , 2012), with an omega-3 to omega-6 fatty acid ratio of 20:1 provided as docosahexaenoic acid (DHA; 22:6n-3; omega-3 fatty acid) and arachidonic acid (AA; 20:4n-6; omega-6 fatty acid). In contrast, an omega-6 fatty acid-rich diet was designed to mimic the standard Western diet, with fat provided as soybean oil and thus containing an omega-6 to omega-3 fatty acid ratio of approximately 8:1 provided as linoleic acid (LA; 18:2n-6; omega-6 fatty acid) and alpha-linolenic acid (ALA; 18:3n-3; omega-3 fatty acid).…”

Section: Resultsmentioning

confidence: 99%

Prolonging the female reproductive lifespan and improving egg quality with dietary omega‐3 fatty acids

et al. 2012

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Summary Women approaching advanced maternal age have extremely poor outcomes with both natural and assisted fertility. Moreover, the incidence of chromosomal abnormalities and birth defects increases with age. As of yet, there is no effective and practical strategy for delaying ovarian aging or improving oocyte quality. We demonstrate that the lifelong consumption of a diet rich in omega-3 fatty acids prolongs murine reproductive function into advanced maternal age, while a diet rich in omega-6 fatty acids is associated with very poor reproductive success at advanced maternal age. Furthermore, even short-term dietary treatment with a diet rich in omega-3 fatty acids initiated at the time of the normal age-related rapid decline in murine reproductive function is associated with improved oocyte quality, while short-term dietary treatment with omega-6 fatty acids results in very poor oocyte quality. Thus, omega-3 fatty acids may provide an effective and practical avenue for delaying ovarian aging and improving oocyte quality at advanced maternal age.

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Docosahexaenoic Acid and Arachidonic Acid Prevent Essential Fatty Acid Deficiency and Hepatic Steatosis

Cited by 27 publications

References 29 publications

Mechanisms of CCl<sub>4</sub>-induced liver fibrosis with combined transcriptomic and proteomic analysis

Mechanisms of CCl<sub>4</sub>-induced liver fibrosis with combined transcriptomic and proteomic analysis

Docosahexaenoic acid, G protein–coupled receptors, and melanoma: is G protein–coupled receptor 40 a potential therapeutic target?

Prolonging the female reproductive lifespan and improving egg quality with dietary omega‐3 fatty acids

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