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Laura den Hartigh, Ph.D.

Metabolism, Endocrinology and Nutrition

Research Assistant Professor of Medicine


Focus

The prevalence of obesity and associated diseases is rapidly reaching epidemic proportions. Representing the major cellular constituent of adipose tissue, adipocytes are now regarded as prominent players in the metabolic as well as hormonal regulation of adiposity. Despite the fundamental role adipose tissue plays in whole body metabolism, nutritive mechanisms that contribute to its maintenance in the context of obesity remain poorly understood. Dr. den Hartigh’s research focuses on the effects of nutrient excess on cellular metabolism, with particular attention given to the effects of fatty acids on cell types associated with the development of obesity such as adipocytes and monocytes/macrophages.



Summary


Dr. den Hartigh received her Ph.D. in Molecular, Cellular, and Integrated Physiology from the University of California, Davis, in 2008, with a Designated Emphasis in Biotechnology.  She began her postdoctoral training in the laboratory of Dr. Dennis Wilson, D.V.M, Ph.D. at the University of California, Davis, and completed her postdoctoral training in the laboratory of Dr. Alan Chait, M.D. at the University of Washington.  She then joined the faculty of the University of Washington as an Acting Instructor in 2013.



Research Interests


My current research investigates the effects of fatty acids on adipocyte lipid metabolism, inflammation, and oxidative stress.  A particular isomer of conjugated linoleic acid, 10E,12Z-CLA, reduces triglyceride storage and increases energy expenditure by adipocytes and has therefore been marketed as a weight loss supplement.  However, in addition to the beneficial effects of reduced adiposity, 10E,12Z-CLA induces detrimental effects such as inflammation and oxidative stress.  We utilize in vitro and murine models to examine the complex effects of 10E,12Z-CLA supplementation on adipocyte biology. 



Publications


Higgins LJ, Rutledge JC.  Inflammation associated with the postprandial lipolysis of triglyceride-rich lipoproteins by lipoprotein lipase.  Curr Atheroscler Rep.  2009 May;11(3):199-205.

Wang L, Gill R, Pederson TL, Higgins LJ, Newman JW, Rutledge JC.  Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial inflammation.  J Lipid Res.  2009 Feb;50(2):204-13.

Tetali SD, Budamagunta MS, Simion C, den Hartigh LJ, Kalai T, Hideg K, Hatters DM, Weisgraber KH, Voss JC, Rutledge JC.  VLDL lipolysis products increase VLDL fluidity and convert apolipoprotein E4 into a more expanded conformation.  J Lipid Res. 2010 Jun;51(6):1273-83.

den Hartigh LJ, Connolly-Rohrbach JE, Fore S, Huser T, Rutledge JC.  Fatty acids from VLDL lipolysis products induce lipid droplet accumulation in human monocytes.  J Immunol.  2010 April 1; 184(7):3927-36. 

den Hartigh LJ, Lame MW, Tablin F, Wilson DW.  Endotoxin and polycyclic aromatic hydrocarbons in ambient fine particulate matter from Fresno, California initiate human monocyte inflammatory responses mediated by reactive oxygen species.  Toxicology in Vitro 24 (2010) 1993–2002.

Weeks T, Schie I, den Hartigh LJ, Rutledge JC, Huser T.  Lipid-cell interactions in human monocytes investigated by doubly-resonant coherent anti-Stokes Raman (DR-CARS) microscopy.  Journal of Biomedical Optics (2011) Feb;16(2):021117.

Han CY, Umemoto T, Omer M, den Hartigh LJ, Chiba T, Leboeuf R, Buller CL, Sweet IR, Pennathur S, Abel ED, Chait A.  NADPH oxidase-derived reactive oxygen species increases expression of monocyte chemotactic factor genes in cultured adipocytes.  J Biol Chem 2012 Mar 23;287(13):10379-93.

Tablin F, den Hartigh LJ, Aung HH, Lame MW, Kleeman MJ, Ham W, Norris JW, Pombo M, Wilson DW.  Seasonal influences on CAPs exposures: Differential responses in platelet activation, serum cytokines, and xenobiotic expression.  Inhal Toxicol 2012 Jul;24(8):506-17.

den Hartigh LJ, Altman R, Hutchinson R, Petrlova J, Budamagunta MS, Tetali SD, Lagerstedt JO, Voss JC, Rutledge JC.  Postprandial apoE isoform and conformational changes associated with VLDL lipolysis products modulate monocyte inflammation.  PLoS ONE 2012;7(11):e50513.