レシチンアシル基転移酵素、レシチンアシルトランスフェラーゼ
- 関
- lecithin cholesterol acyltransferase、phosphatidylcholine-sterol O-acyltransferase
WordNet
- a yellow phospholipid essential for the metabolism of fats; found in egg yolk and in many plant and animal cells; used commercially as an emulsifier
PrepTutorEJDIC
- レシチン(神経細胞や卵黄などに含まれるリン脂質)
UpToDate Contents
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English Journal
- Scavenger Receptor BI and High-Density Lipoprotein Regulate Thymocyte Apoptosis in Sepsis.
- Guo L1, Zheng Z, Ai J, Howatt DA, Mittelstadt PR, Thacker S, Daugherty A, Ashwell JD, Remaley AT, Li XA.Author information 1From the Department of Pediatrics (L.G., Z.Z., J.A., X.-A.L.), Graduate Center for Nutritional Sciences (Z.Z., J.A., X.-A.L.), and Saha Cardiovascular Research Center (D.A.H., A.D., X.-A.L.), University of Kentucky College of Medicine, Lexington; and Laboratory of Immune Cell Biology, National Cancer Institute (P.R.M., J.D.A.) and Lipoprotein Metabolism Section, National Heart, Lung, and Blood Institute (S.T., A.T.R.), National Institutes of Health, Bethesda, MD.AbstractOBJECTIVE: Thymocyte apoptosis is a major event in sepsis; however, how this process is regulated remains poorly understood.
- Arteriosclerosis, thrombosis, and vascular biology.Arterioscler Thromb Vasc Biol.2014 Mar 6. [Epub ahead of print]
- OBJECTIVE: Thymocyte apoptosis is a major event in sepsis; however, how this process is regulated remains poorly understood.APPROACH AND RESULTS: Septic stress induces glucocorticoids production which triggers thymocyte apoptosis. Here, we used scavenger receptor BI (SR-BI)-null mice, which are comp
- PMID 24603680
- Lipid-lowering effect of molluscan (Katelysia opima) glycosaminoglycan (GAG) in hypercholesterolemic induced rats.
- Pandian V, Aravindan N, Subramanian S, Somasundaran ST.AbstractAbstract Identifying pharmacologically safe lipid-lowering 'deliverables' could potentiate therapeutic outcome for diet-induced atherogenesis. Accordingly, we investigated the potential of molluscan (Katelysia opima) glycosaminoglycan (GAG) in modulating the early lipid changes in atherogenesis. Wistar rats were fed a diet with (n=24) or without (n=6) hypercholesterolemic atherogenic CCT (rat chow supplemented with 4% cholesterol, 1% cholic acid, and 0.5% thiouracil) for 17 days. CCT-fed rates were (i) treated with isolated molluscan GAG (40 mg/kg/day, s.c.) for 10 days after the introduction of CCT diet, (ii) cotreated with GAG (40 mg/kg/day, s.c.) for 17 days, or (iii) treated with heparin (200 units/kg/day, s.c.) for 10 days after the introduction of CCT. The increases induced by CCT diet in the plasma levels of cholesterol, triglycerides, high-density lipoprotein, very-low-density lipoprotein, and low-density lipoprotein were completely attenuated with GAG treatment. Consistently, alterations induced by CCT diet in the levels of plasma lecithin cholesterol acyltransferase and lipoprotein lipase activities were restored to baseline levels with GAG treatment. Coherently, histology revealed a decrease associated with GAG treatment in the CCT-diet-induced foam cells (in aorta), tubular damages (kidney), and lipid accumulations (liver). Together, these results suggest that GAG may exert antiatherogenesis potential by significantly attenuating lipid modulations derived by a high-fat diet. Further, the data imply that the GAG extracts may comprehensively prevent hypercholesterolemia-associated tissue damage and could thus serve as a therapeutic deliverable for hypercholesterolemia.
- Biological chemistry.Biol Chem.2014 Mar 1;395(3):355-64. doi: 10.1515/hsz-2013-0214.
- Abstract Identifying pharmacologically safe lipid-lowering 'deliverables' could potentiate therapeutic outcome for diet-induced atherogenesis. Accordingly, we investigated the potential of molluscan (Katelysia opima) glycosaminoglycan (GAG) in modulating the early lipid changes in atherogenesis. Wis
- PMID 24150207
- Anti-psoriatic therapy recovers high-density lipoprotein composition and function.
- Holzer M1, Wolf P2, Inzinger M2, Trieb M1, Curcic S1, Pasterk L1, Weger W2, Heinemann A1, Marsche G1.Author information 1Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.2Department of Dermatology, Medical University of Graz, Graz, Austria.AbstractPsoriasis is a chronic inflammatory disorder associated with increased cardiovascular mortality. Psoriasis affects high-density lipoprotein (HDL) composition, generating dysfunctional HDL particles. However, data regarding the impact of anti-psoriatic therapy on HDL composition and function are not available. HDL was isolated from 15 psoriatic patients at baseline and after effective topical and/or systemic anti-psoriatic therapy and from 15 age- and sex-matched healthy controls. HDL from psoriatic patients showed a significantly impaired capability to mobilize cholesterol from macrophages (6.4 vs. 8.0% [(3)H]cholesterol efflux, P<0.001), low paraoxonase (217 vs. 350 μM(-1) minute(-1) mg(-1) protein, P=0.011) and increased Lp-PLA2 activities (19.9 vs. 12.1 nM(-1) minute(-1) mg(-1) protein, P=0.028). Of particular interest, the anti-psoriatic therapy significantly improved serum lecithin-cholesterol acyltransferase activity and decreased total serum lipolytic activity but did not affect serum levels of HDL-cholesterol. Most importantly, these changes were associated with a significantly improved HDL-cholesterol efflux capability. Our results provide evidence that effective anti-psoriatic therapy recovers HDL composition and function, independent of serum HDL-cholesterol levels, and support to the emerging concept that HDL function may be a better marker of cardiovascular risk than HDL-cholesterol levels.
- The Journal of investigative dermatology.J Invest Dermatol.2014 Mar;134(3):635-42. doi: 10.1038/jid.2013.359. Epub 2013 Aug 28.
- Psoriasis is a chronic inflammatory disorder associated with increased cardiovascular mortality. Psoriasis affects high-density lipoprotein (HDL) composition, generating dysfunctional HDL particles. However, data regarding the impact of anti-psoriatic therapy on HDL composition and function are not
- PMID 23985995
Japanese Journal
- Altered Expression of Both β-Carotene 15,15'Monooxygenase and Lecithin : Retinol Acyltransferase in Obese Zucker Rats
- TAKITANI Kimitaka,MIYAZAKI Hiroshi,FUKUNISHI Shinya,TAKAYA Ryuzo,YODEN Atsushi,HIGUCHI Kazuhide,TAMAI Hiroshi
- Journal of nutritional science and vitaminology 57(1), 108-113, 2011-02-01
- … We examined the expression of genes for β-carotene 15,15 monooxygenase (BCM), lecithin:retinol acyltransferase (LRAT), cellular retinol binding protein-I (CRBP-I), and cytochrome P450 26A1 (CYP26A1) in fa/fa rats and lean control rats. …
- NAID 10028106443
- 眼科図譜(358)LCAT(lecithin-cholesterol acyltransferase)欠損症に伴った角膜混濁の1例
Related Links
- lecithin–cholesterol acyltransferase /lec·i·thin–cho·les·ter·ol ac·yl·trans·fer·ase/ (LCAT) (kah-les´ter-ol a″sil-trans´fer-ās) an enzyme that catalyzes the formation of cholesteryl esters in high-density lipoproteins; deficiency of enzyme ...
- lecithin–cholesterol acyltransferase /lec·i·thin–cho·les·ter·ol ac·yl·trans·fer·ase/ (LCAT) (kah-les´ter-ol a″sil-trans´fer-ās) an enzyme that catalyzes the formation of cholesteryl esters in high-density lipoproteins; deficiency of enzyme ...
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★リンクテーブル★
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- 英
- lecithin acyltransferase、lecithin cholesterol acyltransferase
- 関
- レシチン・コレステロールアシルトランスフェラーゼ、ホスファチジルコリン・ステロール-O-アシルトランスフェラーゼ、レシチンアシル基転移酵素、レシチン・コレステロールアシル基転移酵素
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ホスファチジルコリン・ステロール-O-アシル転移酵素、ホスファチジルコリン・ステロール-O-アシルトランスフェラーゼ
- 関
- lecithin acyltransferase、lecithin cholesterol acyltransferase
[★]
- 英
- lecithin acyltransferase
- 関
- レシチンアシルトランスフェラーゼ
[★]
レシチンアシルトランスフェラーゼ欠損症
- 関
- LCAT deficiency
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アシルトランスフェラーゼ、アシル転移酵素、アシル基転移酵素
- 関
- transacylase