Research Faculty

1150 Saint Nicholas Ave.
Room 238B
New York, NY 10032

Phone: 212-851-5333
Education and Training
S.B. 2000, Mass. Institute of Technology
Ph.D. 2007, University of Michigan

Naomi Berrie Diabetes Center
Rebecca A. Haeusler, Ph.D
Assistant Professor of Pathology and Cell Biology
Research Summary

Cardiovascular disease is the leading cause of death in the United States, and two of its most pervasive risk factors are diabetes and the metabolic syndrome. The prevalence of obesity and diabetes has more than doubled in the US since 1980, and is continuing to climb. However, the tight link between insulin resistance and cardiovascular disease remains, in large part, unexplained. Thus a critical, unanswered question faces the diabetes field: what combination of factors causes the excess coronary disease in these patients? The overall goal of the research in the Haeusler Lab is to understand the development of pro-atherogenic metabolic abnormalities in the natural history of diabetes and the metabolic syndrome.

Questions we aim to address:
How do abnormalities in hepatic lipid metabolism develop during insulin resistance?
How are these abnormalities related to defects in glucose metabolism?
Are bile acids signaling molecules that link insulin resistance to metabolic abnormalities?

Keywords that describe our work:
Metabolism, insulin action, bile acids, triglycerides, cholesterol, glucose, mouse models, lipoproteins, metabolic flux, physiology, pathophysiology, HDL, LDL, diabetes, atherosclerosis, cardiovascular disease, insulin resistance

Welcome to the Haeusler Lab >>>
Selected Publications

Haeusler RA, Camastra S, Nannipieri M, Astiarraga G, Castro-Perez J, Xie D, Wang L, Chakravarthy M, Ferrannini E. (2016) Increased Bile Acid Synthesis and Impaired Bile Acid Transport in Human Obesity. J Clin Endocrinol Metab 101:1935

Ferrannini E, Camastra S, Astiarraga G, Nannipieri M, Castro-Perez J, Xie D, Wang L, Chakravarthy M, Haeusler RA. (2015) Increased Bile Acid Synthesis and Deconjugation after Biliopancreatic Diversion. Diabetes doi:10.2337/db15-0214

Haeusler RA, Camastra S, Astiarraga B, Nannipieri M, Anselmino N, and Ferranini E. (2014) Decreased Expression of Hepatic Glucokinase in Type 2 Diabetes. Molecular Metab. 4: 222

Haeusler RA, Hartil K, Vaitheesvaran B, Arrieta-Cruz I, Knight CM, Cook JR, Kammoun HL, Febbraio MA, Gutierrez-Juarez R, Kurland IJ, and Accili D. (2014) Integrated control of hepatic lipogenesis versus glucose production requires FoxO transcription factors. Nature Commun. 5: 5190

Haeusler RA, Astiarraga B, Camastra S, Accili D, and Ferrannini E. (2013) Human Insulin Resistance is Associated with Increased Plasma Levels of 12-Hydroxylated Bile Acids. Diabetes. 62: 4184

Haeusler RA, Pratt-Hyatt M, Welch CL, Klaassen CD, and Accili D. (2012) Impaired Generation of 12-Hydroxylated Bile Acids Links Hepatic Insulin Signaling with Dyslipidemia. Cell Metab. 15: 65-74

Ai D, Chen C, Han S, Ganda A, Murphy AJ, Haeusler RA, Thorp E, Accili D, Horton JD, and Tall AR. (2012) Regulation of hepatic LDL receptors by mTORC1 and PCSK9. J Clin Invest. 122: 1262

Banks AS, Kim-Muller JY, Mastracci TL, Kofler NM, Qiang L, Haeusler RA, Jurczak MJ, Laznik D, Heinrich G, Samuel VT, Shulman GI, Papaioannou VE, and Accili D. (2011) Dissociation of the Glucose and Lipid Regulatory Functions of FoxO1 by Targeted Knockin of Acetylation-Defective Alleles in Mice. Cell Metab. 14: 587-597

Haeusler RA, Kaestner KH, and Accili D. (2010) FoxOs function synergistically to promote glucose production. J. Biol. Chem. 285: 35245-35248

Haeusler RA, Han S, and Accili D. (2010) Hepatic FoxO1 ablation exacerbates lipid abnormalities during hyperglycemia. J. Biol. Chem. 285: 26861-26868.

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