Faculty & Staff
Doctoral Training and Teaching Faculty
Henry N. Ginsberg, M.D.
Irving Professor of Medicine
B.A. 1966, Brooklyn College
M.D. 1970, State University of New York
Dr. Ginsberg conducts research related to the regulation of the levels and metabolism of apolipoprotein B-containing lipoproteins, the lipoproteins carrying triglycerides and the bulk of cholesterol in blood. These include the atherogenic very low density and low density lipoproteins. Dr. Ginsberg has a particular emphasis on the pathophysiology of hypertriglyceridemia and the dyslipidemia associated with insulin resistance and diabetes mellitus. Research is conducted at three levels: tissue culture using both human and rat hepatoma cells, transgenic mice, and human clinical studies. In cultured cells, Dr. Ginsberg and his associates have described the role of lipid substrate availability in determining if newly synthesized a of degradation and lipoprotein assembly of apoB. His group has characterized the role of the proteasome in the degradation of apoB.
In transgenic mice, he had developed a model of insulin resistance and dylipidemia with many characteristics of the human disorder. This model, as well as others now in use in the lab, allow the group to dissect the important components of substrate availability and genetic control that lead to hypertriglyceridemia. Dr. Ginsberg’s group makes and studies transgenic mice, conducting whole body, cellular, and molecular experiments.
In clinical studies, Dr. Ginsberg is investigating postprandial hyperlipidemia as a risk factor in patients with diabetes. He is also part of a group at Columbia that will be studying the role of glycemic, lipid and blood pressure control in the prevention of cardiovascular disease in patients with diabetes. The latter, named the ACCORD trial, is a 10-year trial with 10,000 patients at 6 sites across the United States. Dr. Ginsberg also has a long record of research into the effects of diet on lipid and lipoprotein metabolism in humans, and has conducted numerous controlled feeding studies in humans.
Recent Publications - Pubmed
1. Liang, J-s., Kim, T., Fang, S., Weissman, A.M., Fisher, E.A., and Ginsberg, H.N. (2003) Overexpression of the tumor autocrine motility factor receptor-gp78, a ubiquitin protein ligase (E3), results in increased ubiquitinylation and decreased secretion of apolipoprotein B100 in Hep G2 cells. J Biol Chem 278:23984-8
2. Ginsberg, H.N. and Fisher, E.A. (2002) Complexity in the secretory pathway: The assembly and secretion of apolipoprotein B-containing lipoproteins. J. Biol. Chem 277:17377-80
3. Siri P., Candela, N., Ko, C., Zhang Y., Eusufzai, S., Ginsberg, H.N., and Huang Li-Shin. (2001) Post-transcriptional stimulation of the assembly and secretion of triglyceride-rich apolipoproteinB-lipoproteins in a mouse with selective deficiency of brown adipose tissue, obesity and insulin resistance. J Biol Chem 276:46064-72
4. Liang, J-S., Distler, O., Cooper, D, Jamil, H., Deckelbaum, R.J., Ginsberg, H.N. and Sturley, S.J. (2001) HIV protease inhibitors protect apolipoprotein B from degradation by the proteasome: A potential mechanism for protease inhibitor-induced hyperlipidemia. Nature Medicine 7:1327-31
5. Mitchell, D.M., Zhou, M., Pariyarath, R. Wang, H., Aitchison, J.D. Ginsberg, H.N. and Fisher, E.A. (1998) Apoprotein B has a prolonged interaction with the translocon during which its lipidation and translocation changes from MTP-dependent to MTP-independent. Proc. Natl. Acad. Sci. USA. 95:14733-8
6. Zhou, M.Y., Fisher, E.A., Ginsberg, H.N. (1998) Regulatable co-translational ubiquitination of apolipoprotein B:100: A new paradigm for proteasomal degradation of a secretory protein. J. Biol. Chem. 38:24649-53