Our Research: Faculty/Research Laboratories

Alan Chait, MD

Edwin L. Bierman Professor of Medicine

Head, Division of Metabolism, Endocrinology and Nutrition

Email Address: achait@u.washington.edu

Division of Metabolism, Endocrinology and Nutrition Website:  http://depts.washington.edu/metab/

Alan Chait, MD

Background:

Dr. Chait received his MBChB (MD equivalent) and his MD (PhD equivalent) from the University of Cape Town, South Africa. After completing an internship at Groote Schuur Hospital in Cape Town, he finished his residency and a research fellowship at the Hammersmith Hospital, Royal Postgraduate Medical School, in London, UK. He next became a lecturer in Endocrinology at the London Hospital. He came to the UW as a senior research fellow in Metabolism and Endocrinology in 1975, and was appointed to the faculty in 1977. In 1985 he was appointed Professor of Medicine, and became Head of the Division on Metabolism, Endocrinology and Nutrition in 1996. In addition to clinical teaching and patient care responsibilities at the University of Washington Medical Center, since 1977 Dr. Chait has been funded by the NIH and other sources to study mechanisms of atherogenesis, with a particular focus on the role of diabetes in the pathogenesis of macrovascular disease. He has served as Director of the UW’s Clinical Nutrition Research Unit (CNRU) – recently renamed Nutrition Obesity Research Center (NORC) from 1992 till 2012, and until recently has been a PI for a Program Project to study macrovascular disease in diabetes. He also is the PI on a NIH T32 Training Grant from the NHLBI. He is a member of the American Society for Clinical Investigation and the Association of American Physicians, and serves on several editorial boards.

Focus:

Dr. Chait’s research focuses on lipoprotein-proteoglycan interactions in atherogenesis; the role of diabetes in the pathogenesis of macrovascular disease; and the links amongst obesity, inflammation, insulin resistance and atherosclerosis.

Lipoprotein-proteoglycan interactions in atherogenesis
The interaction of atherogenic lipoproteins with vascular proteoglycans is a critical step in the initiation of atherogenesis.  Lipoproteins that are retained by these matrix molecules can undergo various modifications that make then potentially more atherogenic.  The Chait lab is studying molecular determinants that alter the interaction of lipoproteins with proteoglycans.  These include factors that modify proteoglycan structure so as to alter their ability to interact with lipoproteins, and apolipoprotein determinants of proteoglycan binding.  As part of these studies the Chait lab has discovered that serum amyloid A (SAA), an inflammatory protein that is transported mainly on HDL, can bind vascular proteoglycans and lead to retention of SAA-containing lipoproteins in the artery wall.  Studies are being performed to determine whether SAA plays a direct role in mediating atherosclerosis, or is simply a marker of the inflammation that is part of the atherogenic process.

Diabetes in the pathogenesis of macrovascular disease
Diabetes is a major risk factor for the pathogenesis of premature vascular disease.  Our lab is studying potential mechanisms by which diabetes may cause inflammation and stimulate the interaction of lipoproteins with vascular proteoglycans.  In particular, we are interested in the role of SAA in the pathogenesis of diabetic vascular disease.  For these studies we are using mouse models of both type 2 and type 1 diabetes, and will be studying the effect of SAA deficiency, and overexpression of various inducible SAA isoforms by macrophages in the artery wall.  These studies should provide important insights into the link between inflammation and lipoprotein-vascular wall interactions in the pathogenesis of atherosclerosis in diabetes.

Obesity, inflammation, insulin resistance and atherosclerosis
Inflammation of visceral adipose tissue is associated with insulin resistance, systemic inflammation and atherosclerosis.  Adipose tissue inflammation is characterized by macrophage accumulation.  Our lab is using in vitro approaches to understand mechanisms by which adipocytes become activated to produce chemotactic factors that recruit macrophages.  We are particularly interested in the role of excess nutrients derived from glucose or various fatty acids, and of dietary cholesterol.  We also use mouse models to study how obesity and nutrient excess leads to adipose tissue and systemic inflammation, and how this inflammation in turn can accelerate atherogenesis.  As part of this work, we are studying how inflammation affects HDL composition and function.

Representative Publications:

Han, C.Y., Umemoto, T., Omer, M., Den Hartigh, L.J., Chiba, T., Leboeuf, R., Buller, C.L., Sweet, I.R., Pennathur, S., Abel, E.D., Chait, A.: NADPH oxidase-derived reactive oxygen species increases expression of monocyte chemotactic factor genes in cultured adipocytes. J. Biol. Chem. 287:10379-93, 2012.

Ding, Y., Subramanian, S., Montes, V., Goodspeed, L., Wang, S., Han, C.Y., Sta. Teresa III, A., Kim, J., O’Brien, K., Chait, A.: Toll-like receptor 4 deficiency decreases atherosclerosis but does not protect against inflammation in obese LDL receptor-deficient mice. Arterioscler. Thromb. Vasc. Biol. 32:1596-1604, 2012.

Umemoto, T., Subramanian, S., Ding, Y., Goodspeed, L., Wang, S., Han, C.Y., Sta. Teresa, A., Kim, J., O’Brien, K., Chait, A.: Inhibition of intestinal cholesterol absorption decreases atherosclerosis but not adipose tissue inflammation. J. Lipid Res. 53:2380-2389, 2012.

Tateya, S., Rizzo-De Leon, N., Handa, P., Cheng, A., Morgan-Stevenson, V., Ogimoto, K., Kanter, J., Bornfeldt, K., Daum, G., Clowes, A., Chait, A., Kim, F.: VASP increases hepatic fatty acid oxidation by activating AMPK in mice. Diabetes. 62:1913-22, 2013.

Umemoto, T., Han, C.Y., Mitra, P., Averill, M., Tang, C., Goodspeed, L., Omer, M., Subramanian, S., Wang, S., den Hartigh, L., Wei, H., Kim, E., Kim, J., O’Brien, K., Chait, A.: Apolipoprotein A-I and HDL have anti-inflammatory effects on adipocytes via cholesterol transporters: ATP-binding cassette (ABC) A-1, ABCG-1 and scavenger receptor B-1(SRB-1). Circ. Res. 112:1345-54, 2013.

Montes, V., Turner, M., Subramanian, S., Ding, Y., Hayden-Ledbetter, M., Slater, S., Goodspeed, L., Wang, S., Omer, M., den Hartigh, L., Averill, M., O’Brien, K., Ledbetter, J., Chait, A.: T cell activation inhibitors reduce CD8+ T cell and pro-inflammatory macrophage accumulation in adipose tissue of obese mice. PLoS ONE 8(7):e67709. doi:10.1371/journal.pone.0067709, 2013.

Subramanian, S., Turner, M., Ding, Y., Goodspeed, L., Wang, S., Buckner, J., O’Brien, K., Getz, G., Reardon, C., Chait, A.: Increased levels of invariant natural killer T lymphocytes worsens metabolic abnormalities and atherosclerosis in obese mice. J. Lipid Res. 54:2831–41, 2013.

den Hartigh, L., Han, C., Wang, S., Omer, M., Chait, A.: 10E, 12Z-conjugated linoleic acid impairs adipocyte triglyceride storage by enhancing fatty acid oxidation, lipolysis, and mitochondrial reactive oxygen species. J. Lipid Res. 54:2964-78, 2013.

  • Boren J, Olin K, Lee I, Chait A, Wight TN, Innerarity TL:  Identification of the principal proteoglycan-binding site in LDL:  A single point mutation in apo B100 severely affects proteoglycan interaction without affecting LDL receptor binding.  J Clin Invest 101:2658-2664, 1998.

    Chang MY, Olin K, Tsoi C, Wight TN, Chait A:  Human monocyte-derived macrophages secrete two forms of proteoglycan-macrophage colony stimulating factor  that differ in their ability to bind low density lipoproteins.  J Biol Chem 273:15985-15992, 1998.

    Crawford RS, Kirk EA, Rosenfeld ME, LeBoeuf RC, Chait A:  Dietary antioxidants inhibit the development of fatty streak lesions in the LDL receptor-deficient mouse.  Arterioscler Thromb Vasc Biol 18:1506-1513, 1998.

    O’Brien KD, Olin KL, Alpers CE, Chiu W, Ferguson M, Hudkins K, Wight TN, Chait A:  A comparison of apolipoprotein and proteoglycan deposits in human coronary athero-sclerotic plaques:  Co-localization of biglycan with apolipoproteins. Circulation 98:519-527, 1998.

    Crawford RS, Mudaliar SR, Henry RR, Chait A:  Inhibition of low density lipoprotein oxidation in vitro but not ex vivo by troglitazone.  Diabetes 48:783-790, 1999.

    Olin KL, Potter-Perigo S, Barrett H, Wight TN, Chait A:  Lipoprotein lipase enhances the binding of native and oxidized low density lipoproteins to versican and biglycan synthesized by cultured arterial smooth muscle cells.  J Biol Chem 274:34629-34636, 1999.

    Kawamura M, Heinecke JW, Chait A:  Increased uptake of alpha-hydroxy aldehyde modified low density lipoprotein by macrophage scavenger receptors.  J Lipid Res41:1054-1059, 2000.

    Chang MY, Potter-Perigo S, Tsoi C, Chait A, Wight TN:  Oxidized low density lipoproteins regulate synthesis of monkey aortic smooth muscle cell proteoglycans that have enhanced native low density lipoprotein binding properties.  J Biol Chem 275:4766-4773, 2000.

    Chait A, Wight TN:  Interaction of native and modified low-density lipoproteins with extracellular matrix.  Curr Opin Lipidol 11:457-463, 2000.

    Olin KL, Potter-Perigo S, Barrett PH, Wight TN, Chait A:  Biglycan, a vascular proteoglycan, binds differently to HDL(2) and HDL(3): role of apoE.  Arterioscler Thromb Vasc Biol21:129-135, 2001.

    Chang MY, Potter-Perigo S, Wight TN, Chait A:  Oxidized LDL bind to nonproteoglycan components of smooth muscle extracellular matrices.  J Lipid Res 42:824-833, 2001.

    Brown BG, Zhao XQ, Chait A, Fisher LD, Cheung MC, Morse JS, Dowdy AA, Marino EK, Bolson EL, Alaupovic P, Frohlich J, Albers JJ:  Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease.  N Engl J Med345:1583-1592, 2001.

    Tannock LR, Little PJ, Wight TN, Chait A:  Arterial smooth muscle cell proteoglycans synthesized in the presence of glucosamine demonstrate reduced binding to LDL.  J Lipid Res 43:149-157, 2002.

    Tannock LR, Olin KL, Barrett PH, Wight TN, Chait A:  Triglyceride-rich lipoproteins from subjects with type 2 diabetes do not demonstrate increased binding to biglycan, a vascular proteoglycan.  J Clin Endocrinol Metab 87:35-40, 2002.

    Little PJ, Tannock LR, Olin KL, Chait A., Wight TN:  Proteoglycans synthesized by arterial smooth muscle cells in the presence of transforming growth factor-beta1 exhibit increased binding to LDLs.  Arterioscler Thromb Vasc Biol 22:55-60, 2002.

    Olin-Lewis, KL Benton, JL, Rutledge JC, Baskin DG, Wight TN, Chait A:  Apolipoprotein E mediates the retention of high density lipoproteins by mouse carotid arteries and cultured arterial smooth muscle cell extracellular matrices.  Circ Res 90:1333-1339, 2002.

    Olin-Lewis KL., Krauss RM, La Belle M, Blanche PJ, Barrett PHR, Wight TN, Chait A:  Apo C-III content of apo B-containing lipoproteins is associated with binding to the vascular proteoglycan, biglycan.  J Lipid Res 43:1969-77, 2002.

    Meyers CD, Tannock LR, Wight TN, Chait A:  Statin-exposed vascular smooth muscle cells secrete proteoglycans with decreased binding affinity for LDL.  J Lipid Res 44:2152-2160, 2003.

    Vidal J, Verchere CB, Andrikopoulos S, Wang F, Hull RL, Cnop M, Olin KL, LeBoeuf RC, O’Brien KD, Chait A, Kahn SE:  The effect of apolipoprotein E deficiency on islet amyloid deposition in human islet amyloid polypeptide transgenic mice.  Diabetologia 46:71-79, 2003.

    Chang MY, Tsoi C, Wight TN, Chait A:  Lysophosphatidylcholine regulates synthesis of biglycan and the proteoglycan form of macrophage colony stimulating factor. Arterioscler Thromb Vasc Biol 23:809-815, 2003.

    Herbst KL, Tannock LR, Deeb SS, Purnell JQ, Brunzell JD, Chait A:  Kobberling type of familial partial lipodystrophy: an underrecognized syndrome.  Diab Care 26:1819-1824, 2003.

    O’Brien KD, Vuletic S, McDonald TO, Wolfbauer G, Lewis K, Tu AY, Marcovina S, Wight TN, Chait A, Albers JJ:  Cell-associated and extracellular phospholipid transfer protein in human coronary atherosclerosis.  Circulation 108:270-274, 2003.

    Lewis KE, Kirk EA, McDonald TO, Wang S, Wight TN, O’Brien KD, Chait A:  Increase in serum amyloid A evoked by dietary cholesterol is associated with increased atherosclerosis in mice.  Circulation 110:540-545, 2004.

    Renard CB, Kramer F, Johansson F, Lamharzi N, Tannock LR, von Herrath MG, Chait A, Bornfeldt KE:  Diabetes and diabetes-associated lipid abnormalities have distinct effects on initiation and progression of atherosclerotic lesions.  J Clin Invest 114:659-668, 2004.

    Lamharzi N, Renard CB, Kramer F, Pennathur S, Heinecke JW, Chait A, Bornfeldt KE:  Hyperlipidemia in concert with hyperglycemia stimulates the proliferation of macrophages in atherosclerotic lesions: potential role of glucose-oxidized LDL.  Diabetes 53:3217-3225, 2004.

    Bergt C, Pennathur S, Fu X, Byun J, O’Brien K, McDonald TO, Singh P, Chait A, Brunzell J, Geary RL, Oram JF, Heinecke JW:  The myeloperoxidase product hypochlorous acid oxidizes HDL in the human artery wall and impairs ABCA1-dependent cholesterol transport.  Proc Natl Acad Sci USA 101:13032-13037, 2004.

    O’Brien KD, Lewis K, Fischer JW, Johnson P, Hwang JY, Knopp EA, Kinsella M, Barrett PHR, Chait A, Wight TN:  Smooth muscle cell biglycan overexpression results in increased lipoprotein retention on extracellular matrix:  implications for the retention of lipoproteins in atherosclerosis.  Atherosclerosis 177:29-35, 2004.

    Chait A, Han CY, Oram JF, Heinecke JW:  Thematic review series:  The immune system and atherogenesis.  Lipoprotein-associated inflammatory proteins: markers or mediators of cardiovascular disease?  J Lipid Res 46:389-403, 2005.

    Tannock LR, O’Brien KD, Knopp RH, Retzlaff B, Fish B, Wener MH, Kahn SE, Chait A:  Cholesterol feeding increases C-reactive protein and serum amyloid A levels in lean insulin-sensitive subjects.  Circulation 111:3058-3062, 2005.

    O’Brien KD, McDonald TO, Kunjathoor V, Eng K, Knopp EA, Lewis K, Lopez R, Kirk EA, Chait A, Wight TN, deBeer FC, LeBoeuf RC:  Serum amyloid A and lipoprotein retention in murine models of atherosclerosis.  Arterioscler Thromb Vasc Biol 25:785-790, 2005.

    Chang MY, Han CY, Wight TN, Chait A:  Antioxidants inhibit the ability of lysophosphatidylcholine to regulate proteoglycan synthesis.  Arterioscler Thromb Vasc Biol26:494-500, 2006.

    Takeshita J, Byun J, Nhan TQ, Pritchard DK, Pennathur S, Schwartz SM, Chait A, Heinecke JW:  Myeloperoxidase generates 5-chlorouracil in human atherosclerotic tissue:  A potential pathway for somatic mutagenesis by macrophages.  J Biol Chem 281:3096-3104, 2006.

    O’Brien KD, Chait A: Serum Amyloid A:  the “other” inflammatory protein.  Curr Atheroscler Rep 8:62-68, 2006.

    Han CY, Chiba T, Campbell JS, Fausto N, Chaisson M, Orasanu G, Plutzky J, Chait A:  Reciprocal and co-ordinate regulation of serum amyloid A versus apolipoprotein A-I and paraoxonase-1 by inflammation in murine hepatocytes.  Arterioscler Thromb Vasc Biol26:1806-1813, 2006.

    Tannock LR, Kirk EA, King VL, LeBoeuf R, Wight TN, Chait A:  Glucosamine supplementation accelerates early but not late atherosclerosis in LDL receptor-deficient mice.  J Nutr 36:2856-2861, 2006.

    Coenen KR, Gruen ML, Chait A, Hasty AH:  Diet-induced increases in adiposity, but not plasma lipids, promote macrophage infiltration into white adipose tissue.  Diabetes56:564-573, 2007.

    Chira EC, McMillen TS, Wang S, Haw A 3rd, O’Brien KD, Wight TN, Chait A:  Tesaglitazar, a dual peroxisome proliferator-activated receptor alpha/gamma agonist, reduces atherosclerosis in female low density lipoprotein receptor deficient mice.  Atherosclerosis195:100-109, 2007.

    McDonald TO, Gerrity RG, Jen C, Chen HJ, Wark K, Wight TN, Chait A, O’Brien KD:  Diabetes and arterial extracellular matrix changes in a porcine model of atherosclerosis.  J Histochem Cytochem 55:1149-1157, 2007.

    Han CY, Subramanian S, Chan CK, Omer M, Chiba T, Wight TN, Chait A:  Adipocyte-derived serum amyloid A3 and hyaluronan play a role in monocyte recruitment and adhesion.  Diabetes 56:2260-2273, 2007.

    Vaisar T, Pennathur S, Green PS, Gharib SA, Hoofnagle AN, Cheung MC, Byun J, Vuletic S, Kassim S, Singh P, Chea H, Knopp RH, Brunzell J, Geary R, Chait A, Zhao XQ, Elkon K, Marcovina S, Ridker P, Oram JF, Heinecke JW:   Shotgun proteomics implicates protease inhibition and complement activation in the antiinflammatory properties of HDL.  J Clin Invest 117:746-756, 2007.

    Saraswathi V, Gao L, Morrow JD, Chait A, Niswender KD, Hasty AH:  Fish oil increases cholesterol storage in white adipose tissue with concomitant decreases in inflammation, hepatic steatosis, and atherosclerosis in mice.  J Nutr 137:1776-1782, 2007.

    Coenen KR, Gruen ML, Chait A, Hasty AH:  Diet-induced increases in adiposity, but not plasma lipids, promote macrophage infiltration into white adipose tissue.  Diabetes56:564-573, 2007.

    Johansson F, Kramer F, Barnhart S, Kanter JE, Vaisar T, Merrill RD, Geng L, Oka K, Chan L, Chait A, Heinecke J, Bornfeldt K:  Type 1 diabetes promotes disruption of advanced atherosclerotic lesions in LDL receptor-deficient mice.  Proc Natl Acad Sci 105:2082-2087, 2008.

    Subramanian S, Han CY, Chiba T, McMillen TS, Wang SA, Haw A, Kirk EA, O’Brien KD, Chait A:  Dietary cholesterol worsens adipose tissue macrophage accumulation and atherosclerosis in obese LDL receptor-deficient mice.  Arterioscler Thromb Vasc Biol 28:685-691, 2008.

    Chiba T, Shinozaki S, Nakazawa T, Kawakami A, Ai M, Kaneko E, Kitagawa M, Kondo K, Chait A, Shimokado K:  Leptin deficiency suppresses progression of atherosclerosis in apoE-deficient mice.  Atherosclerosis 196:68-75, 2008.

    Mazzone T, Chait A, Plutzky J:  Cardiovascular disease risk in type 2 diabetes mellitus:  Insights from mechanistic studies.  Lancet 371:1800-1809, 2008.

    Kim F, Pham M, Maloney E, Rizzo NO, Morton GJ, Wisse BE, Kirk EA, Chait A, Schwartz MW:  Vascular inflammation, insulin resistance, and reduced nitric oxide production precede the onset of pheripheral insulin resistance.  Arterioscler Thromb Vasc Biol28:1982-8, 2008.

    Chiba, T., Shinozaki, S., Nakazawa T., Kawakami, A., Ai, M., Kaneko, E., Kitagawa, M., Kondo, K., Chait, A., Shimokado, K.:  Leptin deficiency suppresses progression of atherosclerosis in apoE-deficient mice.  Atherosclerosis 196:68-75, 2008.

    Subramanian, S., Chait, A.:  The effect of dietary cholesterol on macrophage accumulation in adipose tissue:  Implications for systemic inflammation and atherosclerosis.  Curr Opin Lipidol 20:39-44, 2009.

    Chait, A., Bornfeldt, K.E.:  Diabetes and atherosclerosis:  Is there a role for hyperglycemia?  J Lipid Res 50:S335-S339, 2009.

    Chiba, T., Han, C.Y., Vaisar, T., Shimokado, K., Kargi, A., Chen M.H., Wang, S., McDonald, T.O., O’Brien K.D., Heinecke, J.W., Chait, A.: Serum amyloid A3 does not contribute to circulating SAA levels.  J Lipid Res 50:1353-1362, 2009.

    Zhao, X.Q., Krasuski, R.A., Baer, J., Whitney, E.J., Neradilek, B., Chait, A., Marcovina, S., Albers, J.J., and Brown, B.G.,: Effects of combination lipid therapy on coronary stenosis progression and clinical cardiovascular events in coronary disease patients with metabolic syndrome: A combined analysis of the familial atherosclerosis treatment study (FATS), the HDL-Atherosclerosis treatment study (HATS), and the armed forces regression study (AFREGS).  Am J Cardiol 104:1457-1464, 2009.

    Han, C.Y., Kargi, A.Y., Omer, M., Chan, C.K., Wabitsch, M., O’Brien, K.D., Wight, T.N., Chait, A.: Differential effect of saturated and unsaturated free fatty acids on the generation of monocyte adhesion and chemotactic factors by adipocytes: dissociation of adipocyte hypertrophy from inflammation. Diabetes 59:386-396, 2010.

    Yoon, J., Subramanian, S., Ding, Y., Wang, S., Goodspeed, L., Sullivan, B., Kim, J., O’Brien, K., Chait, A.: Chronic insulin therapy reduces adipose tissue macrophage content in LDL-receptor-deficient mice. Diabetologia 54:1252-60, 2011.

    Chiba, T., Chang, M., Wang S., Wight T., McMillen T., Oram J., Vaisar T., Heinecke J., DeBeer, F., De Beer, M., Chait, A.: Serum amyloid A facilitates the binding of high-density lipoprotein from mice injected with lipopolysaccharide to vascular proteoglycans. Arterioscler. Thromb. Vasc. Biol., 31:1326-32, 2011.

    Subramanian, S., Goodspeed, L., Wang, S., Kim, J., Zeng, L., Ioannou, G., Haigh, W., Yeh, M., Kowdley, K., O’Brien, K., Pennathur, S., Chait, A.: Dietary cholesterol exacerbates hepatic steatosis and inflammation in obese LDL receptor-deficient mice. J Lipid Res., 52:1626-35. 2011.

    Han, C.Y., Umemoto, T., Omer, M., Den Hartigh, L.J., Chiba, T., Leboeuf, R., Buller, C.L., Sweet, I.R., Pennathur, S., Abel, E.D., Chait, A.: NADPH oxidase-derived reactive oxygen species increases expression of monocyte chemotactic factor genes in cultured adipocytes. J. Biol. Chem. 287:10379-93, 2012.

    Ding, Y., Subramanian, S., Montes, V., Goodspeed, L., Wang, S., Han, C.Y., Sta. Teresa III, A., Kim, J., O’Brien, K., Chait, A.: Toll-like receptor 4 deficiency decreases atherosclerosis but does not protect against inflammation in obese LDL receptor-deficient mice. Arterioscler. Thromb. Vasc. Biol. 32:1596-1604, 2012.

    Umemoto, T., Subramanian, S., Ding, Y., Goodspeed, L., Wang, S., Han, C.Y., Sta. Teresa, A., Kim, J., O’Brien, K., Chait, A.: Inhibition of intestinal cholesterol absorption decreases atherosclerosis but not adipose tissue inflammation. J. Lipid Res. 53:2380-2389, 2012.

    Tateya, S., Rizzo-De Leon, N., Handa, P., Cheng, A., Morgan-Stevenson, V., Ogimoto, K., Kanter, J., Bornfeldt, K., Daum, G., Clowes, A., Chait, A., Kim, F.: VASP increases hepatic fatty acid oxidation by activating AMPK in mice. Diabetes. 62:1913-22, 2013.

    Umemoto, T., Han, C.Y., Mitra, P., Averill, M., Tang, C., Goodspeed, L., Omer, M., Subramanian, S., Wang, S., den Hartigh, L., Wei, H., Kim, E., Kim, J., O’Brien, K., Chait, A.: Apolipoprotein A-I and HDL have anti-inflammatory effects on adipocytes via cholesterol transporters: ATP-binding cassette (ABC) A-1, ABCG-1 and scavenger receptor B-1(SRB-1). Circ. Res. 112:1345-54, 2013.

    Montes, V., Turner, M., Subramanian, S., Ding, Y., Hayden-Ledbetter, M., Slater, S., Goodspeed, L., Wang, S., Omer, M., den Hartigh, L., Averill, M., O’Brien, K., Ledbetter, J., Chait, A.: T cell activation inhibitors reduce CD8+ T cell and pro-inflammatory macrophage accumulation in adipose tissue of obese mice. PLoS ONE 8(7):e67709. doi:10.1371/journal.pone.0067709, 2013.

    Subramanian, S., Turner, M., Ding, Y., Goodspeed, L., Wang, S., Buckner, J., O’Brien, K., Getz, G., Reardon, C., Chait, A.: Increased levels of invariant natural killer T lymphocytes worsens metabolic abnormalities and atherosclerosis in obese mice. J. Lipid Res. 54:2831–41, 2013.

    den Hartigh, L., Han, C., Wang, S., Omer, M., Chait, A.: 10E, 12Z-conjugated linoleic acid impairs adipocyte triglyceride storage by enhancing fatty acid oxidation, lipolysis, and mitochondrial reactive oxygen species. J. Lipid Res. 54:2964-78, 2013.

     

     

Current Collaborations:

Within the Diabetes and Obesity Center of Excellence and its Affiliated Members
Jay Heinecke, MD
Tomas Vaisar, PhD
Karin Bornfeldt, PhD
Francis Kim, MD
William Osborne, PhD
Renee LeBoeuf, PhD

Outside of the Diabetes and Obesity Center of Excellence
Kevin O’Brien, MD, University of Washington
Elaine Raines, University of Washington
Michael Rosenfeld, PhD, University of Washington
Thomas Wight, PhD, Benaroya Research Institute
Frederic DeBeer, MD, University of Kentucky
Godfrey Getz, MD, University of Chicago
Nikolaus Marx, MD, University of Ulm

Lab Members:

Savitha Subramaniam, MD
Chang Yeop Han, PhD
Vince Montes, MD
Laura den Hartigh, PhD
Shari Wang
Mohamed Omer
Leela Goodspeed