共查询到20条相似文献,搜索用时 15 毫秒
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A crucial role of sterol regulatory element-binding protein-1 in the regulation of lipogenic gene expression by polyunsaturated fatty acids 总被引:19,自引:0,他引:19
Yahagi N Shimano H Hasty AH Amemiya-Kudo M Okazaki H Tamura Y Iizuka Y Shionoiri F Ohashi K Osuga J Harada K Gotoda T Nagai R Ishibashi S Yamada N 《The Journal of biological chemistry》1999,274(50):35840-35844
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Dual regulation of mouse Delta(5)- and Delta(6)-desaturase gene expression by SREBP-1 and PPARalpha. 总被引:8,自引:0,他引:8
Takashi Matsuzaka Hitoshi Shimano Naoya Yahagi Michiyo Amemiya-Kudo Tomohiro Yoshikawa Alyssa H Hasty Yoshiaki Tamura Jun-ichi Osuga Hiroaki Okazaki Yoko Iizuka Akimitsu Takahashi Hirohito Sone Takanari Gotoda Shun Ishibashi Nobuhiro Yamada 《Journal of lipid research》2002,43(1):107-114
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Docosahexaenoic acid (DHA) and hepatic gene transcription 总被引:1,自引:0,他引:1
Jump DB Botolin D Wang Y Xu J Demeure O Christian B 《Chemistry and physics of lipids》2008,153(1):3-13
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Pachikian BD Essaghir A Demoulin JB Neyrinck AM Catry E De Backer FC Dejeans N Dewulf EM Sohet FM Portois L Deldicque L Molendi-Coste O Leclercq IA Francaux M Carpentier YA Foufelle F Muccioli GG Cani PD Delzenne NM 《PloS one》2011,6(8):e23365
Patients with non-alcoholic fatty liver disease are characterised by a decreased n-3/n-6 polyunsaturated fatty acid (PUFA) ratio in hepatic phospholipids. The metabolic consequences of n-3 PUFA depletion in the liver are poorly understood. We have reproduced a drastic drop in n-3 PUFA among hepatic phospholipids by feeding C57Bl/6J mice for 3 months with an n-3 PUFA depleted diet (DEF) versus a control diet (CT), which only differed in the PUFA content. DEF mice exhibited hepatic insulin resistance (assessed by euglycemic-hyperinsulinemic clamp) and steatosis that was associated with a decrease in fatty acid oxidation and occurred despite a higher capacity for triglyceride secretion. Microarray and qPCR analysis of the liver tissue revealed higher expression of all the enzymes involved in lipogenesis in DEF mice compared to CT mice, as well as increased expression and activation of sterol regulatory element binding protein-1c (SREBP-1c). Our data suggest that the activation of the liver X receptor pathway is involved in the overexpression of SREBP-1c, and this phenomenon cannot be attributed to insulin or to endoplasmic reticulum stress responses. In conclusion, n-3 PUFA depletion in liver phospholipids leads to activation of SREBP-1c and lipogenesis, which contributes to hepatic steatosis. 相似文献
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Jump DB 《Current opinion in lipidology》2008,19(3):242-247
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Kang SA Hong K Jang KH Kim YY Choue R Lim Y 《The Journal of nutritional biochemistry》2006,17(6):419-426
Levan or high molecular beta-2,6-linked fructose polymer is produced extracellularly from sucrose-based substrates by bacterial levansucrase. In the present study, to investigate the effect of levan feeding on serum leptin, hepatic lipogenic enzyme and peroxisome proliferation-activated receptor (PPAR) alpha expression in high-fat diet-induced obese rats, 4-week-old Sprague-Dawley male rats were fed high-fat diet (beef tallow, 40% of calories as fat), and, 6 weeks later, the rats were fed 0%, 1%, 5% or 10% levan-supplemented diets for 4 weeks. Serum leptin and insulin level were dose dependently reduced in levan-supplemented diet-fed rats. The mRNA expressions of hepatic fatty acid synthase and acetyl CoA carboxylase, which are the key enzymes in fatty acid synthesis, were down-regulated by dietary levan. However, dietary levan did not affect the gene expression of hepatic malic enzyme, phosphatidate phosphohydrolase and HMG CoA reductase. Also, the lipogenic enzyme gene expression in the white adipose tissue (WAT) was not affected by the diet treatments. However, hepatic PPARalpha mRNA expression was dose dependently up-regulated by dietary levan, whereas PPARgamma in the WAT was not changed. The results suggest that the in vivo hypolipidemic effect of dietary levan, including anti-obesity and lipid-lowering, may result from the inhibition of lipogenesis and stimulation of lipolysis, accompanied with regulation of hepatic lipogenic enzyme and PPARalpha gene expression. 相似文献
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The role of liver X receptor-alpha in the fatty acid regulation of hepatic gene expression 总被引:7,自引:0,他引:7
Pawar A Botolin D Mangelsdorf DJ Jump DB 《The Journal of biological chemistry》2003,278(42):40736-40743
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Ségolène Arnauld Marco Fidaleo Marie-Claude Clémencet Grégory Chevillard Anne Athias Joseph Gresti Ronald J. Wanders Norbert Latruffe Valérie Nicolas-Francès Stéphane Mandard 《Biochimie》2009,91(11-12):1376-1386
The peroxisomal 3-ketoacyl-CoA thiolase B (Thb) gene was previously identified as a direct target gene of PPARalpha, a nuclear hormone receptor activated by hypolipidemic fibrate drugs. To better understand the role of ThB in hepatic lipid metabolism in mice, Sv129 wild-type and Thb null mice were fed or not the selective PPARalpha agonist Wy14,643 (Wy).Here, it is shown that in contrast to some other mouse models deficient for peroxisomal enzymes, the hepatic PPARalpha signaling cascade in Thb null mice was normal under regular conditions. It is of interest that the hypotriglyceridemic action of Wy was reduced in Thb null mice underlining the conclusion that neither thiolase A nor SCPx/SCP2 thiolase can fully substitute for ThB in vivo. Moreover, a significant increased in the expression of lipogenic genes such as Stearoyl CoA Desaturase-1 (SCD1) was observed in Thb null mice fed Wy. Elevation of Scd1 mRNA and protein levels led to higher SCD1 activity, through a molecular mechanism that is probably SREBP1 independent. In agreement with higher SCD1, enrichment of liver mono-unsaturated fatty acids of the n-7 and n-9 series was found in Thb null mice fed Wy.Overall, we show that the reduced peroxisomal β-oxidation of fat observed in Thb null mice fed Wy is associated with enhanced hepatic lipogenesis, through the combined elevation of microsomal SCD1 protein and activity. Ultimately, not only the amount but also the quality of the hepatic fatty acid pool is modulated upon the deletion of Thb. 相似文献
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