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 continuously 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) since 1992, is a PI for a Program Project to study macrovascular disease in diabetes, is the Project Leader on another Program Project Grant, and 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. He also chairs the US-Japan Nutrition and Metabolism Panel of the US-Japan Cooperative Medical Science Program.

Dr. Chait’s clinical work focuses on endocrinology care at the UWMC Endocrinology Clinic and treatment of lipid disorders at the HMC Lipid Clinic.

The focus of the laboratory is on investigation of the cell biology of atherosclerosis, with particular emphasis on the roles of atherogenic lipoproteins, diabetes mellitus, and inflammation.  The molecular determinants of lipoprotein retention by extracellular matrix molecules secreted by vascular smooth muscle cells and macrophages is being studied using cell culture techniques, animal models and specimens of human arteries.  An additional aspect of interest relates to how inflammatory signals alter adipocyte biology and lipoprotein composition and function, and how these changes might play a role in atherogenesis.

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.

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.

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.

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 coordinate regulation of serum amyloid A versus apolipoprotein A-I and paraoxonase-1 by inflammation in murine hepatocytes.  Arterioscler Thromb Vasc Biol 26:1806-1813, 2006.

Chang MY, Han CY, Wight TN, Chait A:  Antioxidants inhibit the ability of lysophosphatidylcholine to regulate proteoglycan synthesis. Arterioscler Thromb Vasc Biol 26:494-500, 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 136:2856-2861, 2006.

Chira EC, McMillen TS, Wang S, Haw A III, 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.  Atherosclerosis 2007 Jan 8; [Epub ahead of print]

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 2007 Mar 14; [Epub ahead of print]

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 2007 Jun 11; [Epub ahead of print]

Subramanian, S., Han, C.Y., Chiba, T., McMillen, T.S., Wang, S.A., Haw, A., Kirk, E.A., O’Brien, K.D., 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.

Mazzone, T., Chait A., Plutzky, J.:  Cardiovascular disease risk in type 2 diabetes mellitus: insights from mechanistic studies.  Lancet 371(9626): 1800-1809, 2008.

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.

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.