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Post by Max on Jun 27, 2005 14:19:33 GMT -5
The PPAR isoforms
The PPARs (Peroxisome proliferator-activated receptors) are forming a part of the steroidal superfamily of receptors [1]. PPARgamma, a receptor subtype, is accompanied by a selective upregulation of several adipogenic and lipogenic genes including adipose differentiation-related protein (ADRP), adipocyte fatty acid-binding protein 4, sterol regulatory element-binding protein-1 (SREBP-1), fatty acid synthase (FAS), and acetyl-CoA carboxylase [2].
Significant inhibition of the Fatty acid synthase
In rats, fatty acid synthase (FAS), one of the main lipogenic enzymes, converts dietary calories into a storage form of energy. The transcription factors, stimulatory proteins 1 and 3 (Sp1 and Sp3), nuclear factor Y (NF-Y), upstream stimulatory factor (USF) and sterol regulatory element binding protein-1 (SREBP-1) have cognate binding sites on the promoter of the FAS gene [9].
(Ro)accutane induced inhibition of sterol regulatory binding protein-1 (SREBP-1) function and inhibition of lipoprotein lipase activity
Sterol regulatory element-binding protein-1 (SREBP-1) is a transcription factor which regulates genes involved in the synthesis of fatty acids and triglycerides [3]. Significantly elevated levels of triglycerides, low density lipoproteins and cholesterol have been found in human subjects exposed to retinoic acid, (Ro)accutane, in repeated studies [4, 5 and more]. SREBP-1c is also found to be coregulated by RXR-LXR receptors in mice [10]. Cholesterol metabolism is tightly controlled by members of the sterol regulatory element-binding protein (SREBP) family of transcription factors [14].
Inhibition of the lipoprotein lipase (LPL)
Isotretinoin significantly reduced the fat elimination rate as measured by IVFTT (p less than 0.001) and also decreased the muscle lipoprotein lipase activity (LPLA) (p less than 0.05) [15]. Some studies during the 1980s have denied (Ro)accutane induced significant inhibition of the lipoprotein lipase [16 and more]. The lipoprotein lipase contains promoter regions for Sp1 and SREBP and is therefore with highest certainity affected by (Ro)accutane. An evolutionarily conserved 5'-CCTCCCCCC-3' motif (from -91 to -83, CT element) in the human LPL gene promoter is found. Deletion or mutation caused approximately 70-80% decrease in promoter activity. In the lipoprotein lipase promoter, Sp1 and Sp3 in THP-1 nuclear protein extracts bind specifically to this element. Co-transfection with Sp1 and Sp3 expression plasmids transactivated the LPL promoter via the CT element in Drosophila SL2 cells devoid of Sp proteins. Sp3 moderately repressed Sp1-mediated LPL promoter activation when both were co-expressed in SL2 cells. Furthermore, co-expression of an active sterol regulatory element binding protein (SREBP-1), with Sp1, but not with Sp3, synergistically activated the LPL promoter in SL2 cells.
Significant inhibition of lipoxygenases
Peroxisome proliferator-activated receptor-gamma (PPARgamma) activators inhibit cytokine-stimulated LOX-1 expression [8]. The lipoxygenases catalyze the dioxygenation of polyenoic fatty acids such as linoleate and arachidonate. Lectin-like OxLDL receptor was found to be significantly inhibited in cells exposed to retinoic acid. Both LOX-1 and LOX-2 were found to be significantly inhibited by retinol, 13-cis-retinoic acid and all-trans-retinoic acid. A 50% inhibition of conversion towards linoleic acid (omega 3 isoforms) was observed in doses of 10microM [6]. The expression of LOX-1 affects a variety of gene expression, including adhesion molecules, endothelial constitutive nitric oxide synthetase (eNOS), and monocyte chemoatractant protein-1 (MCP-1) [7].
Resolvins (Rvs) are oxygenated products derived from omega-3 polyunsaturated fatty acids (PUFAs) such as eicosapentaenoic acid (EPA) and docosahexaenoic acid that carry potent protective bioactions present in resolving inflammatory exudates. Resolvin E1 (RvE1) is biosynthesized in vivo from EPA via transcellular biosynthetic routes during cell-cell interactions, and thus RvE1 is formed in vivo during multicellular responses such as inflammation and microbial infections. RvE1 protects tissues from leukocyte-mediated injury and counterregulates proinflammatory gene expression. These newly identified Rvs may underlie the beneficial actions of omega-3 PUFAs especially in chronic disorders where unresolved inflammation is a key mechanism of pathogenesis [12].
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Post by Max on Jun 27, 2005 14:19:48 GMT -5
Inhibition of uptake of Liver-type fatty acid binding protein, L-FABP, and inhibition of cellular uptake of fat
Liver-type fatty acid binding protein (L-FABP) binds with high affinity to hydrophobic molecules including free fatty acid, bile acid and bilirubin, which are potentially nephrotoxic, and is involved in their metabolism mainly in hepatocytes. Circulatory L-FABP was found to be filtered by glomeruli and internalized by PTC probably via megalin-mediated endocytosis. These results suggest a novel renal uptake pathway for L-FABP, a carrier of hydrophobic molecules, some of which may exert nephrotoxic effects [11].
Surfactant-like particles (SLP) are unilamellar secreted membranes associated with the process of lipid absorption and isolated previously only from the apical surface of enterocytes. In rats, cubilin, and its anchoring protein megalin have been identified as components of extracellular SLP, but only cubilin is present to any extent in intracellular SLP. During fat absorption, intestinal alkaline phosphatase (IAP) is modestly enriched in intracellular SLP, but full-length cubilin (migrating at 210 kDa in fat-fed mucosal fractions) falls by one-half, although fragments of cubilin are abundant in the intracellular SLP. Both IAP and cubilin colocalize to the same cells during corn oil absorption and colocalize around lipid droplets [13]. It is here suggested that (Ro)accutane induced downregulation of megalin and cubilin through inhbition of Sp1 and Sp3 promoter acitivity inhibits cellular uptake of fat and transport of lipid droplets through the cellular membrane.
The role of fatty acids
(Ro)accutane induced altered metabolism of fatty acids induce several alterations in various parts of the body, including the brain. It functions as a source of energy and structural components for cells; as a regulator of gene expression that impacts lipid, carbohydrate, and protein metabolism, as well as cell growth and differentiation. Fatty acids interact with the genome through several mechanisms. They regulate the activity or nuclear abundance of several transcription factors, including PPAR, LXR, HNF-4, NFkappaB, and SREBP. Fatty acids or their metabolites bind directly to specific transcription factors to regulate gene transcription. Further definition of these fatty acid-regulated pathways will provide insight into the role dietary fat plays in human health and the onset and progression of several chronic diseases, like coronary artery disease and atherosclerosis, dyslipidemia and inflammation, obesity and diabetes, cancer, major depressive disorders [18].
Conclusion
The fat metabolism is here suggested to be significantly altered in subjects exposed to (Ro)accutane. The toxin is a non-selective PPAR-ligand, while other receptors in the same complex, such as the thyroid receptors (TR) and androgen receptors (AR) are suppressed, resulting in hypometabolism through among other things an inhibition of fat synthesis (through lessened promoter activity of SREBP-1), an alteration of fat storage (via inhibition of FAS) and conversion rates, and a deficiency of omega3 fatty acids (linoleic acids) through PPARgamma mediated inhibition of LOX.
Hoffman la Roche itself sells Xenical a lipoprotein lipase inhibitor, which in itself can be considered a substance filled with doubtful effects on health, such as inhibition of fat uptake and increased circulation of lipoproteins, and should be aware about the exact Sp1 and Sp3 binding sites of the lipoprotein lipase, and an induced significant inhibition by (Ro)accutane.
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Post by Max on Jun 27, 2005 14:20:13 GMT -5
References:
[2] Schadinger SE, Bucher NL, Schreiber BM, Farmer SR. PPARgamma2 regulates lipogenesis and lipid accumulation in steatotic hepatocytes. (2005) Am J Physiol Endocrinol Metab. Jun;288(6):E1195-205. [3] Takahashi A, Shimano H, Nakagawa Y, Yamamoto T, Motomura K, Matsuzaka T, Sone H, Suzuki H, Toyoshima H, Yamada N. Transgenic mice overexpressing SREBP-1a under the control of the PEPCK promoter exhibit insulin resistance, but not diabetes. (2005) Biochim Biophys Acta. Jun 10;1740(3):427-33. [6] Goldreich D, Grossman S, Sofer Y, Breitbart E, Sklan D. The effect of retinol and retinoic acids on lipoxygenase activity. (1997) Int J Vitam Nutr Res. 67(1):4-9. [7] Ohki I, Ishigaki T, Oyama T, Matsunaga S, Xie Q, Ohnishi-Kameyama M, Murata T, Tsuchiya D, Machida S, Morikawa K, Tate S. Crystal Structure of Human Lectin-like, Oxidized Low-Density Lipoprotein Receptor 1 Ligand Binding Domain and Its Ligand Recognition Mode to OxLDL. (2005) Structure (Camb). Jun;13(6):905-17. [8] Ando K, Fujita T. Role of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in the development of hypertensive organ damage. (2004) Clin Exp Nephrol. Sep;8(3):178-82. [9] Schweizer M, Roder K, Zhang L, Wolf SS. Transcription factors acting on the promoter of the rat fatty acid synthase gene. (2002) Biochem Soc Trans. Nov;30(Pt 6):1070-2. [10] Yoshikawa T, Shimano H, Amemiya-Kudo M, Yahagi N, Hasty AH, Matsuzaka T, Okazaki H, Tamura Y, Iizuka Y, Ohashi K, Osuga J, Harada K, Gotoda T, Kimura S, Ishibashi S, Yamada N. Identification of liver X receptor-retinoid X receptor as an activator of the sterol regulatory element-binding protein 1c gene promoter. (2001) Mol Cell Biol. May;21(9):2991-3000. [11] Oyama Y, Takeda T, Hama H, Tanuma A, Iino N, Sato K, Kaseda R, Ma M, Yamamoto T, Fujii H, Kazama JJ, Odani S, Terada Y, Mizuta K, Gejyo F, Saito A. Evidence for megalin-mediated proximal tubular uptake of L-FABP, a carrier of potentially nephrotoxic molecules. (2005) Lab Invest. 2005 Apr;85(4):522-31. [12] Arita M, Clish CB, Serhan CN. The contributions of aspirin and microbial oxygenase to the biosynthesis of anti-inflammatory resolvins: Novel oxygenase products from omega-3 polyunsaturated fatty acids. (2005) Biochem Biophys Res Commun. Aug [13] Mahmood A, Shao JS, Alpers DH. Rat enterocytes secrete SLPs containing alkaline phosphatase and cubilin in response to corn oil feeding. (2003) Am J Physiol Gastrointest Liver Physiol. Aug;285(2):G433-41. [14] Sundqvist A, Ericsson J. Transcription-dependent degradation controls the stability of the SREBP family of transcription factors. (2003) Proc Natl Acad Sci U S A. Nov 25;100(24):13833-8. [15] Vahlquist C, Lithell H, Michaelsson G, Selinus I, Vahlquist A, Vessby B. Plasma fat elimination tissue lipoprotein lipase activity and plasma fatty acid composition during sequential treatment with etretinate and isotretinoin. (1987) Acta Derm Venereol. 67(2):139-44. [16] Bershad S, Rubinstein A, Paterniti JR, Le NA, Poliak SC, Heller B, Ginsberg HN, Fleischmajer R, Brown WV. Changes in plasma lipids and lipoproteins during isotretinoin therapy for acne. (1985) N Engl J Med. Oct 17;313(16):981-5. [17] Yang WS, Deeb SS. Sp1 and Sp3 transactivate the human lipoprotein lipase gene promoter through binding to a CT element: synergy with the sterol regulatory element binding protein and reduced transactivation of a naturally occurring promoter variant. (1998) J Lipid Res. Oct;39(10):2054-64. [18] Jump DB. Fatty acid regulation of gene transcription. (2004) Crit Rev Clin Lab Sci. 41(1):41-78.
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Post by Max on Jul 19, 2005 16:42:10 GMT -5
Mol Cell Proteomics. 2004 Jul;3(7):692-703. Epub 2004 Apr 8. Related Articles, Links
Polyunsaturated fatty acids including docosahexaenoic and arachidonic acid bind to the retinoid X receptor alpha ligand-binding domain.
Lengqvist J, Mata De Urquiza A, Bergman AC, Willson TM, Sjovall J, Perlmann T, Griffiths WJ.
Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE-17177 Stockholm, Sweden.
Nuclear receptors (NRs) constitute a large and highly conserved family of ligand-activated transcription factors that regulate diverse biological processes such as development, metabolism, and reproduction. As such, NRs have become important drug targets, and the identification of novel NR ligands is a subject of much interest. The retinoid X receptor (RXR) belongs to a subfamily of NRs that bind vitamin A metabolites (i.e. retinoids), including 9-cis-retinoic acid (9-cis-RA). However, although 9-cis-RA has been described as the natural ligand for RXR, its endogenous occurrence has been difficult to confirm. Recently, evidence was provided for the existence of a different natural RXR ligand in mouse brain, the highly enriched polyunsaturated fatty acid (PUFA) docosahexaenoic acid (DHA) (Mata de Urquiza et al. (2000) Science 290, 2140-2144). However, the results suggested that supra-physiological levels of DHA were required for efficient RXR activation. Using a refined method for ligand addition to transfected cells, the current study shows that DHA is a more potent RXR ligand than previously observed, inducing robust RXR activation already at low micromolar concentrations. Furthermore, it is shown that other naturally occurring PUFAs can activate RXR with similar efficiency as DHA. In additional experiments, the binding of fatty acid ligands to RXRalpha is directly demonstrated by electrospray mass spectrometry of the noncovalent complex between the RXR ligand-binding domain (LBD) and its ligands. Data is presented that shows the noncovalent interaction between the RXR LBD and a number of PUFAs including DHA and arachidonic acid, corroborating the results in transfected cells. Taken together, these results show that RXR binds PUFAs in solution and that these compounds induce receptor activation, suggesting that RXR could function as a fatty acid receptor in vivo.
PMID: 15073272 [PubMed - indexed for MEDLINE] Biochem Biophys Res Commun. 2004 Oct 22;323(3):1116-23. Related Articles, Links
Peroxisome proliferator-activated receptor alpha ligands activate transcription of lectin-like oxidized low density lipoprotein receptor-1 gene through GC box motif.
Hayashida K, Kume N, Minami M, Inui-Hayashida A, Mukai E, Toyohara M, Kita T.
Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Japan.
Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is a receptor for oxidized LDL. Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors regulating transcription of various genes. We examined effects of PPAR ligands on LOX-1 expression and their transcriptional regulation in vascular endothelial cells. PPARalpha-specific ligands, such as fenofibrate and WY-14643, but not PPARgamma-specific ligands induced LOX-1 expression. Reduced expression of PPARalpha by antisense oligonucleotides directed to PPARalpha blocked fenofibrate-induced LOX-1 expression. Luciferase reporter gene assays with deletion and point mutations in the LOX-1 promoter revealed that transcriptional activity of LOX-1 gene by fenofibrate was localized in the -114/-106 GC box. Electrophoretic mobility shift assays with the radiolabeled GC box sequence showed inducible bands by PPARalpha ligands, which is competitively suppressed by unlabeled GC box motif and by an antibody to PPARalpha. In conclusion, PPARalpha appears to be one of the key regulators that induce LOX-1 expression, utilizing the GC box as a promoter.
PMID: 15381115 [PubMed - indexed for MEDLINE]
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Post by Max on Jul 20, 2005 17:58:32 GMT -5
Endocrinology. 2004 Apr;145(4):1527-38. Epub 2003 Dec 4. Related Articles, Links
Comment in: Endocrinology. 2004 Apr;145(4):1525-6. Tyrosine agonists reverse the molecular defects associated with dominant-negative mutations in human peroxisome proliferator-activated receptor gamma.
Agostini M, Gurnell M, Savage DB, Wood EM, Smith AG, Rajanayagam O, Garnes KT, Levinson SH, Xu HE, Schwabe JW, Willson TM, O'Rahilly S, Chatterjee VK.
Department of Medicine, University of Cambridge, Addenbrooke's Hospital, United Kingdom.
Loss-of-function mutations in the ligand-binding domain of human peroxisome proliferator-activated receptor gamma (PPARgamma) are associated with a novel syndrome characterized by partial lipodystrophy and severe insulin resistance. Here we have further characterized the properties of natural dominant-negative PPARgamma mutants (P467L, V290M) and evaluated the efficacy of putative natural ligands and synthetic thiazolidinedione (TZD) or tyrosine-based (TA) receptor agonists in rescuing mutant receptor function. A range of natural ligands failed to activate the PPARgamma mutants and their transcriptional responses to TZDs (e.g. pioglitazone, rosiglitazone) were markedly attenuated, whereas TAs (e.g. farglitazar) corrected defects in ligand binding and coactivator recruitment by the PPARgamma mutants, restoring transcriptional function comparable with wild-type receptor. Transcriptional silencing via recruitment of corepressor contributes to dominant-negative inhibition of wild type by the P467L and V290M mutants and the introduction of an artificial mutation (L318A) disrupting corepressor interaction abrogated their dominant-negative activity. More complete ligand-dependent corepressor release and reversal of dominant-negative inhibition was achieved with TA than TZD agonists. Modeling suggests a structural basis for these observations: both mutations destabilize helix 12 to favor receptor-corepressor interaction; conversely, farglitazar makes more extensive contacts than rosiglitazone within the ligand-binding pocket, to stabilize helix 12, facilitating corepressor release and transcriptional activation. Farglitazar was a more potent inducer of PPARgamma target gene (aP2) expression in peripheral blood mononuclear cells with the P467L mutation. Having shown that rosiglitazone is of variable and limited efficacy in these subjects, we suggest that TAs may represent a more rational therapeutic approach.
PMID: 14657011 [PubMed - indexed for MEDLINE]
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Post by Max on Jul 25, 2005 8:31:17 GMT -5
J Lipid Res. 1998 Oct;39(10):2054-64. Related Articles, Links
Sp1 and Sp3 transactivate the human lipoprotein lipase gene promoter through binding to a CT element: synergy with the sterol regulatory element binding protein and reduced transactivation of a naturally occurring promoter variant.
Yang WS, Deeb SS.
Department of Genetics, University of Washington, Seattle 98195, USA.
Lipoprotein lipase (LPL) is a key enzyme in lipoprotein and energy metabolism and, therefore, regulation of its expression could have an important bearing on these processes. We have identified an evolutionarily conserved 5'-CCTCCCCCC-3' motif (from -91 to -83, CT element) in the human LPL gene promoter, deletion or mutation of which caused approximately 70-80% decrease in promoter activity. We found that Sp1 and Sp3 in THP-1 nuclear protein extracts bind specifically to this element. Co-transfection with Sp1 and Sp3 expression plasmids transactivated the LPL promoter via the CT element in Drosophila SL2 cells devoid of Sp proteins. Sp3 moderately repressed Sp1-mediated LPL promoter activation when both were co-expressed in SL2 cells. Furthermore, co-expression of an active sterol regulatory element binding protein (SREBP-1), with Sp1, but not with Sp3, synergistically activated the LPL promoter in SL2 cells. We previously reported a naturally occurring T-->G substitution at position -93 of the human LPL promoter which reduces promoter activity by 40-50% in transient transfection assays. In this study, we showed that this substitution results in reduced binding affinity to Sp1/Sp3 and in diminished transactivation by Sp1/Sp3 alone and by the synergistic action of Spl and SREBP-1 In conclusion, recruitment of Sp1/Sp3 by the CT element may play an important role in expression of the human lipoprotein lipase gene. Synergistic transcriptional activation by Sp1 and SREBP-1 may provide a mechanism for cross-talk between cholesterol and triglyceride metabolic pathways.
PMID: 9788252 [PubMed - indexed for MEDLINE]
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Post by Max on Sept 6, 2005 15:47:28 GMT -5
Nippon Ronen Igakkai Zasshi. 2002 May;39(3):264-7. Related Articles, Links
[New oxidized LDL receptors and their functions in atherogenesis]
[Article in Japanese]
Kume N.
Department of Geriatric Medicine, Graduate School of Medicine, Kyoto University.
Oxidized low density lipoprotein (Ox-LDL) appears to play key roles in atherosclerotic progression and plaque rupture. Biological effects of Ox-LDL on vascular cells may, at least in part, be mediated by cell surface receptors for Ox-LDL. Lectin-like oxidized LDL receptor (LOX)-1 and scavenger receptor for phosphatidylserine and oxidized lipoprotein (SR-PSOX) are type II and I membrane glycoprtoeins, respectively, both of which can act as cell-surface endocytosis receptors for atherogenic oxidized LDL (Ox-LDL). LOX-1 expression can dynamically be induced by proinflammatory stimuli, and is detectable in cultured macrophages and activated vascular smooth muscle cells (VSMC), in addition to endothelial cells. LOX-1-dependent uptake of Ox-LDL induced apoptosis of cultured VSMC. In vivo, endothelial cells that cover early atherosclerotic lesions, and intimal macrophages and VSMC in advanced atherosclerotic plaques dominantly express LOX-1. LOX-1 expressed on the cellsurface can be cleaved, in part, and released as soluble molecules, suggesting the diagnostic significance of plasma soluble LOX-1 levels. SR-PSOX appeared to be identical to CXCL16, a novel membrane-anchored chemokine directed to CXCR6-positive lymphocytes, suggesting another role of SR-PSOX as T-cell chemoattractant. In contrast to LOX-1 expressed by a variety of cell types. SR-PSOX expression appeared relatively confined to macrophages in atherogenesis. Taken together, LOX-1 and SR-PSOX may play important roles in atherogenesis and athrosclerotic plaque rupture.
PMID: 12073583 [PubMed - indexed for MEDLINE]
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