Toru Seo

Columbia University, New York City, New York, United States

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Publications (32)164.14 Total impact

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    ABSTRACT: To determine whether n-3 fatty acids (n-3) influence arterial cholesterol delivery and lipoprotein lipase (LpL) levels in insulin-resistant mice. Insulin resistance contributes to risk of cardiovascular disease. It was previously reported that saturated fat (SAT) diets increased, but n-3 diets decreased, arterial low-density lipoprotein (LDL) cholesterol deposition from LDL total and selective uptake; this was associated with increased or decreased arterial LpL, respectively. Insulin receptor transgenic knockout mice (L1) were fed a chow, SAT, or n-3 diet for 12 weeks. Double-fluorescent boron dipyrromethene (BODIPY)-cholesteryl ester (CE) and Alexa dye-labeled human LDL were injected to separately trace LDL-CE and LDL-apolipoprotein B whole particle uptake. In contrast to SAT, n-3 diets markedly reduced all plasma lipids, ameliorating progression of insulin resistance. As opposed to SAT, n-3 reduced arterial LDL uptake, CE deposition, and selective uptake. Disparate patterns of CE deposition between diets were comparable with arterial LpL distribution; SAT induced high LpL levels throughout aortic media; LpL was limited only to intima in n-3-fed mice. n-3 diets diminish arterial LDL-cholesterol deposition in mice with insulin resistance, and this is associated with changes in arterial LpL levels and distribution.
    Arteriosclerosis Thrombosis and Vascular Biology 10/2010; 30(12):2510-7. DOI:10.1161/ATVBAHA.110.215848 · 5.53 Impact Factor
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    ABSTRACT: Omega-3 (n-3) fatty acids are emerging as bioactive agents protective against cardiovascular disease. However, their cellular delivery pathways are poorly defined. Here we questioned whether the uptake of n-3 triglyceride-rich particles (TGRP) is mediated by cell surface proteoglycans (PG) using LDL receptor (LDLR)+/+ and LDLR-/- cell models. LDLR+/+ but not LDLR-/- cells showed higher n-6 over n-3 TGRP uptake. Removal of cell surface proteins and receptors by pronase markedly enhanced the uptake of n-3 but not n-6 TGRP. Lactoferrin blockage of apoE-mediated pathways decreased the uptake of n-6 TGRP by up to 85% (p<0.05) but had insignificant effect on n-3 TGRP uptake. PG removal by sodium chlorate in LDLR+/+ cells substantially reduced n-3 TGRP uptake but had little effect on n-6 TGRP uptake. Thus, while n-6 TGRP uptake is preferentially mediated by LDLR-dependent pathways, the uptake of n-3 TGRP depends more on PG and non-LDLR cell surface anchoring.
    Biochemical and Biophysical Research Communications 02/2010; 392(2):135-9. DOI:10.1016/j.bbrc.2009.12.164 · 2.28 Impact Factor
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    ABSTRACT: Obesity is associated with low-grade inflammation in adipose tissue, which contributes to the development of obesity-related diseases such as insulin resistance, hypertension and arteriosclerosis. Here we developed an animal model that non-invasively monitors inflammation in adipose tissue using in vivo bioluminescent imaging (BLI) technique. In vitro, stimulation with TNFalpha or co-culture with RAW264 macrophages increased bioluminescence in 3T3-L1 adipocytes expressing NF-kappaB-mediated luciferase gene (3T3-L1/NF-kappaB-re-luc2P). In vivo, lipopolysaccharide increased bioluminescence in mice transplanted with 3T3-L1/NF-kappaB-re-luc2P cells. Moreover, light emission derived from implanted cells was significantly higher in diet-induced obese mice transplanted with 3T3-L1/NF-kappaB-re-luc2P than in lean mice. Our results showed that BLI technique and 3T3-L1/NF-kappaB-re-luc2P cells provide a useful approach to non-invasively monitor obesity-induced inflammation in adipose tissue in in vivo.
    Biochemical and Biophysical Research Communications 12/2009; 391(1):674-8. DOI:10.1016/j.bbrc.2009.11.119 · 2.28 Impact Factor
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    ABSTRACT: Triglyceride ingestion releases gut peptides from enteroendocrine cells located in the intestinal epithelia and provides feedback regulations of gastrointestinal function. The precise mechanisms sensing lipids in the intestinal wall, however, are not well characterized. In the current study, we investigated the release of gut peptides following oral triglyceride loading in mice deficient for monoacylglycerol acyltransferase 2 (MGAT2KO) and diacylglycerol acyltransferase 1 (DGAT1KO), enzymes that sequentially re-synthesize triglyceride to secrete as chylomicron at the small intestine. In wild-type (Wt) mice, oral triglyceride loading resulted in hypertriglycemia. In addition, plasma glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) were significantly increased 30 min after triglyceride loading, before decaying in 2 h. In MGAT2KO and DGAT1KO mice, oral triglyceride loading did not result in hypertriglycemia and the increase in GIP was significantly suppressed in both KO mouse strains. In contrast, the increases in plasma GLP-1 and PYY in both KO mouse strains were comparable to Wt mice 30 min after triglyceride loading, however, they remained elevated in DGAT1KO mice even 2 h after triglyceride loading. In parallel to the changes in GLP-1 and PYY, gastric emptying was delayed after oral triglyceride loading in MGAT2KO mice comparably to Wt type mice and was further delayed in DGAT1KO mice. STC-1 and GLUTag, GLP-1-producing intestinal endocrine L-cell lines, displayed a significant level of DGAT1 activity but not MGAT activity. These findings suggest that synthesis and/or secretion of triglyceride-rich lipoproteins play an important role in the release of GIP. Moreover, DGAT1 may directly regulate the release of GLP-1 and PYY in L-cells.
    Biochemical and Biophysical Research Communications 12/2009; 390(3-390):377-381. DOI:10.1016/j.bbrc.2009.08.167 · 2.28 Impact Factor
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    ABSTRACT: Glucose ingestion stimulates the secretion of the incretin hormones, glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1). Despite the critical role of incretins in glucose homeostasis, the mechanism of glucose-induced incretin secretion has not been established. We investigated the underlying mechanism of glucose-induced incretin secretion in vivo in mice. Injection of glucose at 1 g/kg in the upper intestine significantly increased plasma GIP and GLP-1 levels, whereas injection of glucose in the colon did not increase GIP or GLP-1 levels. This finding indicates that the glucose sensor for glucose-induced incretin secretion is in the upper intestine. Coadministration of a sodium-glucose cotransporter-1 (SGLT1) inhibitor, phloridzin, with glucose in the upper intestine blocked glucose absorption and glucose-induced incretin secretion. alpha-methyl-d-glucopyranoside (MDG), an SGLT1 substrate that is a nonmetabolizable sugar, significantly increased plasma GIP and GLP-1 levels, whereas phloridzin blocked these increases, indicating that concomitant transport of sodium ions and glucose (substrate) via SGLT1 itself triggers incretin secretion without the need for subsequent glucose metabolism. Interestingly, oral administration of MDG significantly increased plasma GIP, GLP-1, and insulin levels and reduced blood glucose levels during an intraperitoneal glucose tolerance test. Furthermore, chronic MDG treatment in drinking water (3%) for 13 days reduced blood glucose levels after a 2-h fast and in an oral glucose tolerance test in diabetic db/db mice. Our findings indicate that SGLT1 serves as the intestinal glucose sensor for glucose-induced incretin secretion and that a noncalorigenic SGLT1 substrate ameliorates hyperglycemia by stimulating incretin secretion.
    AJP Endocrinology and Metabolism 10/2009; 297(6):E1358-65. DOI:10.1152/ajpendo.00412.2009 · 4.09 Impact Factor
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    ABSTRACT: Chemerin is a novel peptide that was identified as a natural ligand for ChemR23. As it has been reported to be involved in the regulation of immune responses and adipogenesis, chemerin may have a variety of physiological functions. Chemerin is synthesized as a precursor (prochemerin) and is proteolytically activated and inactivated in sequential steps, which control its physiological roles in a coordinated manner. Chemerin-9 (chemerin148–156) was previously identified as the smallest peptide with low nanomolar potency. However, like mature chemerin, chemerin-9 is rapidly degraded and inactivated in plasma, which has limited the use of chemerin-9 in in vivo experiments. In order to identify stable chemerin analogs that facilitate in vivo studies, we synthesized a series of chemerin-9 analogs and examined intrinsic activity and metabolic stability. We identified an agonistic and metabolically stable chemerin-9 analog (d-Tyr147-[d-Ser151, d-Ala154, Tic155]chemerin148–156) that shows enhanced plasma exposure with prolonged half-life in mice upon intraperitoneal administration. Improvement of metabolic stability resulted in a reduction in the plasma free fatty acid levels in fasted mice, which cannot be accomplished by unstable-mouse chemerin-9. This reduction in plasma free fatty acids reflects the anti-lipolysis activity of chemerin-9 and analogs in mouse primary adipocytes. The discovery of a metabolically stable chemerin analog will facilitate investigation of the pharmacological roles of chemerin in vivo. Moreover, this stable chemerin analog might provide new therapeutic approaches to inflammatory diseases such as asthma and metabolic disorders such as obesity and diabetes where ChemR23 activation may be of benefit.
    Peptides 08/2009; DOI:10.1016/j.peptides.2009.05.030 · 2.61 Impact Factor
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    ABSTRACT: We previously reported that saturated fat (SAT)-enriched diets increase arterial cholesteryl ester (CE) deposition, especially from LDL-selective uptake (SU), and this was associated with increased arterial lipoprotein lipase (LpL). We now question how n-3 fatty acid rich diets influence arterial cholesterol delivery and arterial LpL levels. C57BL/6 mice were fed chow or eucaloric high-fat diets enriched in SAT or fish oil (n-3) for 12 weeks, and then injected with double radiolabeled or fluorescent-labeled human LDL to separately trace LDL-CE and LDL-apoB uptake. SAT and n-3 diets increased plasma cholesterol levels similarly; n-3 diets lowered plasma triglyceride concentrations. SAT increased arterial LDL-SU with significantly higher CE infiltration into aortic media. In contrast, n-3 markedly reduced total LDL uptake and CE deposition and abolished SU with LDL localized only in aortic intima. Disparate patterns of CE deposition between diets were consistent with distribution of arterial LpL-SAT diets induced higher LpL levels throughout the aorta; n-3 diets decreased LpL levels and limited LpL expression to the aortic intima. n-3 rich diets decrease arterial total LDL delivery and abrogate LDL-SU in parallel with changing arterial wall LpL expression and distribution.
    Arteriosclerosis Thrombosis and Vascular Biology 03/2009; 29(4):555-61. DOI:10.1161/ATVBAHA.108.182287 · 5.53 Impact Factor
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    ABSTRACT: Because the mechanisms of (n-3) fatty acid-enriched triglyceride-rich particle [(n-3)-TGRP] uptake are not well characterized, we questioned whether (n-3)-TGRP are removed via "nonclassical" pathways, e.g., pathways other than an LDL receptor and/or involving apolipoprotein E (apoE). Chylomicron-sized model (n-3)-TGRP labeled with [3H]cholesteryl ether were injected into wild-type (WT) and CD36 knockout (CD36-/-) mice at low, nonsaturating and high, saturating doses. Blood clearance of (n-3)-TGRP was determined by calculating fractional catabolic rates. At saturating doses, blood clearance of (n-3)-TGRP was slower in CD36-/- mice relative to WT mice, suggesting that in part CD36 contributes to (n-3)-TGRP uptake. To further examine the potential nonclassical clearance pathways, peritoneal-elicited macrophages from WT and CD36-/- mice were incubated with (n-3)-TGRP in the presence of apoE, lactoferrin, and/or sodium chlorate. Cellular (n-3)-TGRP uptake was measured to test the roles of apoE-mediated pathways and/or proteoglycans. ApoE-mediated pathways compensated in part for defective (n-3)-TGRP uptake in CD36-/- cells. Lactoferrin decreased (n-3)-TGRP uptake in the presence of apoE. Inhibition of cell proteoglycan synthesis by chlorate reduced (n-3)-TGRP uptake in both groups of macrophages, and chlorate effects were independent of apoE. We conclude that although CD36 is involved, it is not the primary contributor to the blood clearance of (n-3)-TGRP. The removal of (n-3)-TGRP likely relies more on nonclassical pathways, such as proteoglycan-mediated pathways.
    Journal of Nutrition 03/2008; 138(2):257-61. · 4.23 Impact Factor
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    ABSTRACT: Sterol regulatory element binding proteins (SREBPs) are key transcription proteins that bind to sterol regulatory elements (SRE) of genes essential for cellular cholesterol and fatty acid homeostasis. Polyunsaturated fatty acids (PUFA) strongly inhibit SREBP processing at post-transcriptional levels. We questioned if delivering PUFA as part of a triglyceride (TG) molecule would have similar effects and efficiency as free non-esterified PUFA. CHO cells stably transfected with an SRE-promoter linked to the luciferase reporter gene were incubated for 8-24 h with linoleic acid (LA) complexed to BSA (molar ratios 0.5-4:1), VLDL-sized trilinolein emulsions (TL, 25-200 microg/ml), and chylomicron-sized soy oil emulsions in the presence and absence of apoE. Effects of LA and TL on decreasing SRE-luciferase activity were similar and dose and time dependent. Both TL and LA significantly and rapidly (<or=2-12 h) reduced SRE-mediated gene expression by up to 75%. At equal fatty acid concentrations, SRE inhibition by TL was as effective as LA. ApoE addition increased inhibition by TL. Inhibition of gene expression was highly correlated to cell TG accumulation. We conclude that TG like fatty acids are rapid and efficient modulators of SRE-mediated gene expression.
    Lipids 10/2007; 42(10):885-91. DOI:10.1007/s11745-007-3093-x · 2.35 Impact Factor
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    ABSTRACT: Regulation of cholesterol metabolism in cultured cells and in the liver is dependent on actions of the LDL receptor. However, nonhepatic tissues have multiple pathways of cholesterol uptake. One possible pathway is mediated by LPL, an enzyme that primarily hydrolyzes plasma triglyceride into fatty acids. In this study, LDL uptake and tissue cholesterol levels in heart and skeletal muscle of wild-type and transgenic mice with alterations in LPL expression were assessed. Overexpression of a myocyte-anchored form of LPL in heart muscle led to increased uptake of LDL and greater heart cholesterol levels. Loss of LDL receptors did not alter LDL uptake into heart or skeletal muscle. To induce LDL receptors, mice were treated with simvastatin. Statin treatment increased LDL receptor expression and LDL uptake by liver and skeletal muscle but not heart muscle. Plasma creatinine phosphokinase as well as muscle mitochondria, cholesterol, and lipid droplet levels were increased in statin-treated mice overexpressing LPL in skeletal muscle. Thus, pathways affecting cholesterol balance in heart and skeletal muscle differ.
    The Journal of Lipid Research 04/2007; 48(3):646-55. DOI:10.1194/jlr.M600301-JLR200 · 4.73 Impact Factor
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    ABSTRACT: Lipid emulsions containing long-chain triglycerides (LCT) and medium chain triglycerides (MCT) are widely used in parenteral nutrition. Recently, fish oil (FO) triglyceride (TG)-derived emulsions are considered therapeutic because of their many beneficial biological modulatory actions. We investigated in mice whether adding 10% FO to an intravenous lipid emulsion with MCT and LCT (MCT:LCT:FO -50:40:10% by wt) would affect particle blood clearance and tissue targeting in comparison to LCT (100% by wt) and MCT:LCT (50:50% by wt) emulsions. The 3 emulsions were labeled with [3H] cholesteryl oleoyl ether and administered by bolus injection (400 microg TG/mouse) to C57BL/6J mice. Contributions of LDL receptor (LDL-R) and LDL-R-related protein to emulsion catabolism were assessed using LDL-R-deficient mice and preinjection of lactoferrin, and the effects of lipoprotein lipase (LPL) were determined by preinjection of heparin and Triton WR 1339. Although fractional catabolic rates did not differ among the 3 emulsions, blood removal at each time point after injection was greater for MCT:LCT:FO particles due to their higher initial margination volume. Compared with MCT:LCT and LCT emulsions, patterns of tissue uptake of the MCT:LCT:FO emulsions were different, e.g. MCT:LCT:FO emulsion particle uptake was lower in heart, adipose tissue, and muscle, and higher in lung, and the removal of MCT:LCT:FO emulsion particles was less dependent on LPL, LDL-R, and lactoferrin-sensitive pathways. These data suggest that the addition of a low percentage of FO to MCT:LCT emulsions substantially changes their particle clearance and tissue uptake mechanisms.
    Journal of Nutrition 12/2006; 136(11):2766-72. · 4.23 Impact Factor
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    ABSTRACT: Accumulating evidence in both humans and animal models clearly indicates that a group of very-long-chain polyunsaturated fatty acids, the n-3 fatty acids (or omega-3), have distinct and important bioactive properties compared with other groups of fatty acids. n-3 Fatty acids are known to reduce many risk factors associated with several diseases, such as cardiovascular diseases, diabetes, and cancer. The mechanisms whereby n-3 fatty acids affect gene expression are complex and involve multiple processes. As examples, n-3 fatty acids regulate 2 groups of transcription factors, such as sterol-regulatory-element binding proteins and peroxisome proliferator-activated receptors, that are critical for modulating the expression of genes controlling both systemic and tissue-specific lipid homeostasis. Modulation of specific genes by n-3 fatty acids and cross-talk between these genes are responsible for many effects of n-3 fatty acids.
    American Journal of Clinical Nutrition 07/2006; 83(6 Suppl):1520S-1525S. · 6.92 Impact Factor
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    Scandinavian Journal of Food & Nutrition 06/2006; 50(1):13-16. DOI:10.1080/17482970601069375
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    ABSTRACT: Plasma LDL levels and atherosclerosis both increase on a saturated fat-rich (SAT) diet. LDL cholesterol delivery to tissue may occur via uptake of the LDL particles or via selective uptake (SU), wherein cholesteryl ester (CE) enters cells without concomitant whole-particle uptake. It is not known how dietary fats might directly affect arterial LDL-CE uptake and whether SU is involved. Thus, mice that are relatively atherosclerosis resistant (C57BL/6) or susceptible to atherosclerosis (apoE) were fed a chow or SAT diet and injected with double radiolabeled or fluorescent-labeled human LDL to independently trace LDL-CE core and whole-particle uptake, respectively. Our results show that a SAT diet increased contributions of SU to total arterial LDL-CE delivery in C57BL/6 and apoE mice. The SAT diet increased plasma fatty acid and cholesterol levels; cholesterol, but not fatty acid, levels correlated with SU, as did the degree of atherosclerosis. Increased SU did not correlate with arterial scavenger receptor class B type I levels but paralleled increased lipoprotein lipase (LPL) levels and LPL distribution in the arterial wall. These studies suggest that arterial LDL-CE delivery via SU can be an important mechanism in vivo and that dietary influences on arterial LPL levels and atherogenesis modulate arterial LDL-CE delivery, cholesterol deposition, and SU.
    Journal of Clinical Investigation 09/2005; 115(8):2214-22. DOI:10.1172/JCI24327 · 13.77 Impact Factor
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    ABSTRACT: This review discusses recent advances in delineating basic mechanisms underlying the beneficial effects of omega-3 fatty acids on health and on disease. While a substantial number of studies have delineated many differences between the biological effects of saturated versus polyunsaturated fatty acids, less is known about the long-chain omega-3 fatty acids commonly present in certain fish oils. In this review, we focus on recent studies relating to basic mechanisms whereby omega-3 fatty acids modulate cellular pathways to exert beneficial effects on promoting health and decreasing risks of certain diseases. We will use, as examples, conditions of the cardiovascular, neurological, and immunological systems as well as diabetes and cancer, and then discuss basic regulatory pathways. Omega-3 fatty acids are major regulators of multiple molecular pathways, altering many areas of cellular and organ function, metabolism and gene expression. Generally, these regulatory events lead to "positive" endpoints relating to health and disease.
    Current Opinion in Lipidology 03/2005; 16(1):11-8. · 5.80 Impact Factor
  • Current Opinion in Lipidology 01/2005; 16(1):11-18. DOI:10.1097/00041433-200502000-00004 · 5.80 Impact Factor
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    ABSTRACT: Sterol-regulatory element-binding proteins (SREBPs) regulate transcription of genes of lipid metabolism. Ceramide decreases transcriptionally active SREBP levels independently of intracellular cholesterol levels. Mechanisms of the ceramide-mediated decrease of SREBP levels were investigated. Experiments were performed in Chinese hamster ovary cells. Inhibition of ceramide synthesis with myriocin, cycloserine, or fumonisin decreases levels of transcriptionally active SREBP and reduces SRE-mediated gene transcription. When ceramide synthesis is increased through exogenous sphingosine or inhibition of sphingosine kinase, SRE-mediated gene transcription is increased. The important role of ceramide synthesis in SRE-mediated gene transcription is confirmed in LY-B cells that do not synthesize ceramide de novo. LY-B cells fail to increase SRE-mediated gene transcription in sterol depletion. Ceramide synthesis correlates with the generation of transcriptionally active SREBP and SRE-mediated gene transcription. Inhibition of ceramide synthesis decreases levels of transcriptionally active SREBP and SRE-mediated gene transcription. It is hypothesized that the process of ongoing ceramide synthesis contributes to the physiological processing of SREBP, perhaps affecting ER-to-Golgi trafficking. Taken together, modification of ceramide synthesis could be a novel target for drug development in the pharmacologic modification of SRE-dependent pathways.
    Arteriosclerosis Thrombosis and Vascular Biology 06/2004; 24(5):943-8. DOI:10.1161/01.atv.0000125703.20434.4d · 5.53 Impact Factor
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    ABSTRACT: Lipid accumulation is associated with cardiac dysfunction in diabetes and obesity. Transgenic mice expressing non-transferable lipoprotein lipase (LpL) with a glycosylated phosphatidyl-inositol (GPI) anchor in cardiomyocytes have dilated cardiomyopathy. However, the mechanisms responsible for lipid accumulation and cardiomyopathy are not clear. Hearts from 3-month-old mice expressing GPI-anchored human LpL (hLpLGPI) mice had increased fatty acid oxidation and heart failure genes and decreased glucose transporter genes. 6-month-old mice had increased mRNA expression and activation of the apoptosis marker caspase-3. Moreover, hLpLGPI hearts had significant cytochrome c release from mitochondria to cytosol. Low density lipoprotein uptake was greater in hLpLGPI hearts, and this was associated with more intracellular apolipoprotein B (apoB). To test whether lipid accumulation in the hLpLGPI heart is reduced by cardiac expression of apoB, hLpLGPI mice were bred with transgenic human apoB (HuB)-expressing mice. Hearts of HuB/hLpLGPI mice had less triglyceride (38%) and free fatty acids (19%), secreted more apoB, and expressed less atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) and more glucose transporter 4 (GLUT4). The increased mortality of the mice was abrogated by the transgenic expression of apoB. Therefore, we hypothesize that cardiac apoB expression improves cardiomyopathy by increasing lipid resecretion from the heart.
    Journal of Biological Chemistry 03/2004; 279(6):4204-11. DOI:10.1074/jbc.M311995200 · 4.60 Impact Factor
  • Atherosclerosis Supplements 09/2003; 4(2):133-133. DOI:10.1016/S1567-5688(03)90571-X · 9.67 Impact Factor
  • Atherosclerosis Supplements 09/2003; 4(2):233-233. DOI:10.1016/S1567-5688(03)90998-6 · 9.67 Impact Factor

Publication Stats

1k Citations
164.14 Total Impact Points


  • 2000–2010
    • Columbia University
      • • Institute of Human Nutrition
      • • Department of Pediatrics
      • • College of Physicians and Surgeons
      • • Department of Medicine
      New York City, New York, United States
  • 2009
    • Tsukuba Research Institute
      Edo, Tōkyō, Japan
  • 2008
    • Mahidol University
      • Faculty of Medicine Siriraj Hospital
      Bangkok, Bangkok, Thailand
  • 2002–2003
    • Vrije Universiteit Brussel
      Bruxelles, Brussels Capital, Belgium
    • University of Freiburg
      Freiburg, Baden-Württemberg, Germany
  • 1999
    • CUNY Graduate Center
      New York City, New York, United States
    • Université Libre de Bruxelles
      Bruxelles, Brussels Capital, Belgium
  • 1998
    • Royal College of Physicians and Surgeons of Glasgow
      Glasgow, Scotland, United Kingdom