We are analyzing https://link.springer.com/article/10.1007/s11745-015-4116-7.

Title:
Sterol O-Acyltransferase 2-Driven Cholesterol Esterification Opposes Liver X Receptor-Stimulated Fecal Neutral Sterol Loss | Lipids
Description:
Statin drugs have proven a successful and relatively safe therapy for the treatment of atherosclerotic cardiovascular disease (CVD). However, even with the substantial low-density lipoprotein (LDL) cholesterol lowering achieved with statin treatment, CVD remains the top cause of death in developed countries. Selective inhibitors of the cholesterol esterifying enzyme sterol-O acyltransferase 2 (SOAT2) hold great promise as effective CVD therapeutics. In mouse models, previous work has demonstrated that either antisense oligonucleotide (ASO) or small molecule inhibitors of SOAT2 can effectively reduce CVD progression, and even promote regression of established CVD. Although it is well known that SOAT2-driven cholesterol esterification can alter both the packaging and retention of atherogenic apoB-containing lipoproteins, here we set out to determine whether SOAT2-driven cholesterol esterification can also impact basal and liver X receptor (LXR)-stimulated fecal neutral sterol loss. These studies demonstrate that SOAT2 is a negative regulator of LXR-stimulated fecal neutral sterol loss in mice.
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Keywords {🔍}

article, pubmed, google, scholar, cas, cholesterol, rudel, acat, liver, brown, sterol, central, kelley, mice, wilson, tomoda, sawyer, res, acyltransferase, davis, inhibitors, soat, receptor, lipid, biol, atherosclerosis, ohshiro, hepatic, oacyltransferase, esterification, fecal, lee, neutral, loss, lipoprotein, chem, temel, matsuda, omura, privacy, cookies, content, warrier, zhang, treatment, cvd, selective, density, transport, thromb,

Topics {✒️}

month download article/chapter bell ta 3rd acute sterol o-acyltransferase soat2-driven cholesterol esterification substantial low-density lipoprotein sterol o-acyltransferase 2 major cholesterol-esterifying enzyme dietary fat-induced alterations hepatic niemann-pick c1 cell-based fluorescence assay androgen-mediated cholesterol metabolism niemann-pick c1 gene repa jj monounsaturated fatty acyl-coenzyme full article pdf apolipoprotein e-deficient mice lysosomal acid lipase reverse cholesterol transport biliary sterol secretion effective cvd therapeutics privacy choices/manage cookies hepatic cholesterol homeostasis davies jp proc natl aca niemann-pick c1 niemann-pick c1 article warrier cholesterol acyltransferase inhibitors central regulator intestinal cholesterol absorption cholesterol esterification cholesterol lowering achieved testicular cholesterol metabolism opposite atherosclerotic potential multiple mechanisms limit hepatic acat2 knock abc1-mediated efflux cholesterol-fed mouse diet-induced hypercholesterolemia european economic area hold great promise stroke statistics—2011 update farese rv jr tissue-specific knockouts modifies hdl metabolism recently patented compounds structure-activity relationship wake forest school ethics declarations conflict fecal excretion

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         description:Statin drugs have proven a successful and relatively safe therapy for the treatment of atherosclerotic cardiovascular disease (CVD). However, even with the substantial low-density lipoprotein (LDL) cholesterol lowering achieved with statin treatment, CVD remains the top cause of death in developed countries. Selective inhibitors of the cholesterol esterifying enzyme sterol-O acyltransferase 2 (SOAT2) hold great promise as effective CVD therapeutics. In mouse models, previous work has demonstrated that either antisense oligonucleotide (ASO) or small molecule inhibitors of SOAT2 can effectively reduce CVD progression, and even promote regression of established CVD. Although it is well known that SOAT2-driven cholesterol esterification can alter both the packaging and retention of atherogenic apoB-containing lipoproteins, here we set out to determine whether SOAT2-driven cholesterol esterification can also impact basal and liver X receptor (LXR)-stimulated fecal neutral sterol loss. These studies demonstrate that SOAT2 is a negative regulator of LXR-stimulated fecal neutral sterol loss in mice.
         datePublished:2016-01-04T00:00:00Z
         dateModified:2016-01-04T00:00:00Z
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            Intestine
            Atherosclerosis
            Esterification
            Lipidology
            Neurochemistry
            Medical Biochemistry
            Nutrition
            Medicinal Chemistry
            Microbial Genetics and Genomics
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      headline:Sterol O-Acyltransferase 2-Driven Cholesterol Esterification Opposes Liver X Receptor-Stimulated Fecal Neutral Sterol Loss
      description:Statin drugs have proven a successful and relatively safe therapy for the treatment of atherosclerotic cardiovascular disease (CVD). However, even with the substantial low-density lipoprotein (LDL) cholesterol lowering achieved with statin treatment, CVD remains the top cause of death in developed countries. Selective inhibitors of the cholesterol esterifying enzyme sterol-O acyltransferase 2 (SOAT2) hold great promise as effective CVD therapeutics. In mouse models, previous work has demonstrated that either antisense oligonucleotide (ASO) or small molecule inhibitors of SOAT2 can effectively reduce CVD progression, and even promote regression of established CVD. Although it is well known that SOAT2-driven cholesterol esterification can alter both the packaging and retention of atherogenic apoB-containing lipoproteins, here we set out to determine whether SOAT2-driven cholesterol esterification can also impact basal and liver X receptor (LXR)-stimulated fecal neutral sterol loss. These studies demonstrate that SOAT2 is a negative regulator of LXR-stimulated fecal neutral sterol loss in mice.
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         Intestine
         Atherosclerosis
         Esterification
         Lipidology
         Neurochemistry
         Medical Biochemistry
         Nutrition
         Medicinal Chemistry
         Microbial Genetics and Genomics
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