Li-Shin Huang, Ph.D.
Research Scientist, Department of Medicine
Homepage [1]
Degrees
B.S., 1979 Fu-Jen University Ph.D., 1984 University of Delaware
Research Interests
Elevated plasma levels of apo B and LDL are associated with a higher risk for developing atherosclerosis and coronary heart disease. Dr. Huang's research directions focus on the study of apo B metabolism in transgenic and knockout mouse models. Three major research projects are ongoing - 1) Genetic regulation of apo B secretion. Transgenic mice expressing human apo B are used to study genetic factors that regulate apo B secretion. These studies utilize primary hepatoctyes, in vivo measure of lipoprotein production, and mouse genetic approaches including fine-mapping analysis and positional cloning techniques to identify genes that regulate the assembly and secretion of apo B-containing lipoproteins. Results derived from these studies will provide means for dietary and/or therapeutic interventions toward regulating plasma apo B levels in patients with high plasma apo B and LDL-cholesterol levels; 2) Atherosclerosis in human apo B transgenic mice. Human apo B transgenic mice, with or without ablation in other genes involved in lipoprotein metabolism, fed a high fat diet, are being treated with various drugs to assess the effect of these drugs on lipoprotein metabolism and the development of atherosclerosis. These studies assess the effects of both nutritional and pharmacological perturbations on lipoprotein metabolism and development of atherosclerosis; 3) Hepatic steatosis and lipid metabolism in insulin-resistant mouse models. Transgenic mice overexpressing PPARgamma or microsomal hydrolases are being generated to elucidate their roles in the development of fatty livers and dyslipidemia associated with insulin-resistance and type 2 diabetes.
Recent Publications - Pubmed [2]
Son, N.H., Park, T.S., Yamashita, H., Yokoyama, M., Huggins, L.A., Okajima, K., Homma, S., Szabolcs, M.J., Huang, L.S., and Goldberg, I.J. Cardiomyocyte expression of PPARgamma leads to cardiac dysfunction in mice. J Clin Invest. 2007. 117:2791-2801.
Reid, B.N., Ables, G.P., Otlivanchik, O., Schoiswohl, G., Zechner, R., Goldberg, I.J., Schwabe, R., Chua, S.C., Jr., and Huang, L.S. 2008. Hepatic overexpression of hormone-sensitive lipase and adipose triglyceride lipase promotes fatty acid oxidation, stimulates direct release of free fatty acids and ameliorates steatosis. J Biol Chem. 2008. 283:13087-13099.
Goldberg, I.J., Yu, Y., Noh, H.L., Wei, J., Huggins, L.A., Rackmill, M.G., Hamai, H., Reid, B.N., Blaner, W.S., and Huang, L.S. 2008. Decreased lipoprotein clearance is responsible for increased cholesterol in streptozotocin treated LDL receptor knockout mice. Diabetes. 2008. 57:1674-1682.
Links:
[1] http://www.cumc.columbia.edu/dept/medicine/prevmedmen.html
[2] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?SUBMIT=y&db=PubMed&term=" Huang LS"[au]