Gene expression modulation of liver energy metabolism by oleoyl-oestrone in overweight rats

2009 ◽  
Vol 30 (2) ◽  
pp. 81-89 ◽  
Author(s):  
María Del Mar Romero ◽  
José Antonio Fernández-López ◽  
Marià Alemany ◽  
Montserrat Esteve
Keyword(s):  
Gene Expression ◽  
Energy Metabolism ◽  
Regulatory Element ◽  
Male Rats ◽  
Glucose Disposal ◽  
Pcr Analysis ◽  
Gene Expressions ◽  
Plasma Parameters ◽  
Element Binding Protein ◽  
Limited Food

We intended to determine how the liver copes with the massive handling of lipids induced by OE (oleoyl-oestrone), as well as to characterize and differentiate the actual OE effects from those that may be only the consequence of decreased food intake. Thus we used male rats treated with oral OE (10 nmol/g per day) compared with a vehicle only PF (pair-fed) group and controls fed ad libitum (vehicle only). Plasma parameters, and total liver lipids, glycogen, DNA and total mRNA were measured. RNA was extracted and used for real-time PCR analysis of the gene expression of enzymes and regulatory factors of liver energy metabolism. Most hepatic proteins showed similar gene expressions in OE and controls, but the differences widened between OE and PF rats, showing that OE effects could not be merely attributed to a lower energy intake. The liver of OE-treated rats largely maintained its ability to mobilize glucose for the synthesis of fats; this was achieved in part by a peculiar combination of regulative modifications that facilitate both fatty acid disposal and restrained glucose utilization under conditions of limited food supply but ample availability of internal energy stores. In conclusion, the results presented suggest that the effect of OE on liver metabolism may be (at least in part) mediated through an insulin-sensitivity-dependent modulation of the expression of SREBP-1c (sterol-regulatory-element-binding protein-1c), resulting in the unique combined effect of mildly increased (or maintained) glucose disposal but also limited enhancement of lipogenesis.

scholarly journals Sterol Regulatory Element-binding Protein-2- and Liver X Receptor-driven Dual Promoter Regulation of Hepatic ABC Transporter A1 Gene Expression

2007 ◽  
Vol 282 (29) ◽  
pp. 21090-21099 ◽  
Author(s):  
Norimasa Tamehiro ◽  
Yukari Shigemoto-Mogami ◽  
Tomoshi Kakeya ◽  
Kei-ichiro Okuhira ◽  
Kazuhiro Suzuki ◽  
...  
Keyword(s):  
Gene Expression ◽  
Abc Transporter ◽  
Binding Protein ◽  
Regulatory Element ◽  
Liver X Receptor ◽  
Promoter Regulation ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Dual Promoter

scholarly journals Transcription Factor Sterol Regulatory Element Binding Protein 2 Regulates Scavenger Receptor Cla-1 Gene Expression

2004 ◽  
Vol 24 (12) ◽  
pp. 2358-2364 ◽  
Author(s):  
Morgan Tréguier ◽  
Chantal Doucet ◽  
Martine Moreau ◽  
Christiane Dachet ◽  
Joëlle Thillet ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Binding Protein ◽  
Regulatory Element ◽  
Scavenger Receptor ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

Erythropoietin Lacking Hypoxia Responsive Element in 3′ Untranslated Region Stimulates Hepatic Erythropoiesis in Anemic Xenopus.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4057-4057
Author(s):  
Youichi Aizawa ◽  
Hironori Nishikawa ◽  
Takehito Okui ◽  
Nami Nogawa-Kosaka ◽  
Nobuyoshi Kosaka ◽  
...  
Keyword(s):  
Gene Expression ◽  
Animal Model ◽  
Binding Capacity ◽  
Mammalian Species ◽  
Normal Liver ◽  
Liver Cells ◽  
Pcr Analysis ◽  
Gene Expressions ◽  
Gene Regulations ◽  
Rbc Count

Abstract Recent studies on EPO-EPOR systems in non-mammalian vertebrate including frog and teleost fishes demonstrate extramedullary adult erythropoiesis instead of bone marrow. In adult Xenopus laevis (African clawed frog), an animal model of hepatic erythropoiesis should give an opportunity for understanding the microenvironment of vascular niche. Therefore, we investigate on erythrocyte development, gene expressions and gene regulations of EPO and EPOR molecules in adult Xenopus liver. In situ hybridization and immunostaining revealed that Xenopus EPOR (xlEPOR) expressing erythrocyte progenitors, which have low hemoglobin content, were localized among liver sinusoids. The maximum number of xlEPOR expressing cells was observed when peripheral RBC count reached a nadir after hemolytic anemia. Flowcytometric analysis of peripheral blood cells and dispersed liver cells using anti-xlEPOR antibodies also indicate that the xlEPOR+ cells in liver were increased as decreasing count of peripheral RBC. After a nadir of RBC count, xlEPOR+ immature nucleated erythrocytes were emerged in the circulation. The count of xlEPOR+ immature erythrocytes was gradually decreased as increasing count of xlEPOR− mature erythrocytes. Since mature erythrocytes are still nucleated in Xenopus, we used xlEPOR molecules as erythroid differentiation marker. Meanwhile real time RT-PCR analysis of Xenopus EPO (xlEPO) mRNA revealed that xlEpo gene expression was significantly induced in anemic liver compared to normal liver. These data suggest that xlEPO-xlEPOR signaling between erythrocyte progenitors and liver cells progress the proliferation and differentiation of erythrocyte progenitors, and the mobilization of immature erythrocytes into the circulation. Our previous study showed that the anemic serum of phenylhydrazine administrated Xenopus contains erythroid colony forming activity; however, there is no information about the relationship between anemia and hypoxia enough to stimulate erythropoiesis in adult Xenopus. In mammalian species, Epo gene expression is upregulated by binding of hypoxia inducible factor-1a (HIF-1a) and ARNT complex to hypoxia response element (HRE) located in 3′ enhancer region of Epo gene. In frog and fishes, EPO mRNAs are expressed even in normoxia condition. In fish Epo genes, consensus HRE sequence (ACGTG) were not found in 3′UTR, as well as the reporter assay failed to show Epo upregulation respond to hypoxia. Since any consensus HRE sequence was not found in 3′ UTR of xlEpo gene, we examined whether HIF-1a mediates xlEpo gene regulation. By western blot analysis of HIF-1a, we assessed whether HIF-1a is stabilized in anemia; meanwhile binding capacity of HIF-1a to 5′, 3′ UTRs and intron regions of xlEpo gene was analyzed by gel shift mobility assay. The findings in non-mammalian animal model demonstrate the basis of erythropoietic gene regulations, as well as molecular mechanism underlying adult extramedullary erythropoiesis.

scholarly journals Human Sterol Regulatory Element-Binding Protein 1a Contributes Significantly to Hepatic Lipogenic Gene Expression

2015 ◽  
Vol 35 (2) ◽  
pp. 803-815 ◽  
Author(s):  
Andreas Bitter ◽  
Andreas K. Nüssler ◽  
Wolfgang E. Thasler ◽  
Kathrin Klein ◽  
Ulrich M. Zanger ◽  
...  
Keyword(s):  
Gene Expression ◽  
Human Liver ◽  
Target Genes ◽  
Binding Protein ◽  
Regulatory Element ◽  
Lipogenic Gene ◽  
Knock Down ◽  
Lipogenic Gene Expression ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

Background/Aims: Sterol regulatory element-binding protein (SREBP) 1, the master regulator of lipogenesis, was shown to be associated with non-alcoholic fatty liver disease, which is attributed to its major isoform SREBP1c. Based on studies in mice, the minor isoform SREBP1a is regarded as negligible for hepatic lipogenesis. This study aims to elucidate the expression and functional role of SREBP1a in human liver. Methods: mRNA expression of both isoforms was quantified in cohorts of human livers and primary human hepatocytes. Hepatocytes were treated with PF-429242 to inhibit the proteolytic activation of SREBP precursor protein. SREBP1a-specifc and pan-SREBP1 knock-down were performed by transfection of respective siRNAs. Lipogenic SREBP-target gene expression was analyzed by real-time RT-PCR. Results: In human liver, SREBP1a accounts for up to half of the total SREBP1 pool. Treatment with PF-429242 indicated SREBP-dependent auto-regulation of SREBP1a, which however was much weaker than of SREBP1c. SREBP1a-specifc knock-down also reduced significantly the expression of SREBP1c and of SREBP-target genes. Regarding most SREBP-target genes, simultaneous knock-down of both isoforms resulted in effects of only similar extent as SREBP1a-specific knock-down. Conclusion: We here showed that SREBP1a is significantly contributing to the human hepatic SREBP1 pool and has a share in human hepatic lipogenic gene expression.

scholarly journals FoxO1 Inhibits Sterol Regulatory Element-binding Protein-1c (SREBP-1c) Gene Expression via Transcription Factors Sp1 and SREBP-1c

2012 ◽  
Vol 287 (24) ◽  
pp. 20132-20143 ◽  
Author(s):  
Xiong Deng ◽  
Wenwei Zhang ◽  
InSug O-Sullivan ◽  
J. Bradley Williams ◽  
Qingming Dong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Binding Protein ◽  
Regulatory Element ◽  
Element Binding Protein ◽  
Sterol Regulatory Element
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