Rebecca Anne Haeusler, PhD

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Overview

Academic Appointments

  • Assistant Professor of Pathology and Cell Biology

Credentials & Experience

Education & Training

  • BS, 2000 Biology, Massachusetts Institute of Technology
  • PhD, 2007 Biological Chemistry, University of Michigan

Research

The goals of our research are to understand the development of proatherogenic metabolic abnormalities in insulin resistant individuals, and to identify new therapeutic targets for improving these abnormalities. Two current areas of focus are dysregulation of (i) lipoprotein and (ii) bile acid metabolism. Lipoproteins carry out atherogenic and atheroprotective actions, and may link insulin resistance with cardiovascular disease. Bile acids are involved in maintaining cholesterol, glucose, and triglyceride homeostasis, and are dysregulated during insulin resistance and diabetes. Through these two research areas, we aim to determine mechanisms of metabolic abnormalities and atherogenesis in the natural history of type 2 diabetes, and to identify potential therapeutic targets.

Welcome to Haeusler Lab.

Research Interests

  • Development of pro-atherogenic metabolic abnormalities in history of diabetes, metabolic syndrome

Selected Publications

Higuchi S, Ahmad TR, Argueta DA, Perez PA, Zhao C, Schwartz GJ, DiPatrizio NV, Haeusler RA. (2020) Bile acid composition regulates GPR119-dependent intestinal lipid sensing and food intake regulation in mice Gut http://dx.doi.org/10.1136/gutjnl-2019-319693

Ahmad TR and Haeusler RA. (2019) Bile acids in glucose metabolism and insulin signaling: mechanisms and research needs Nat Rev Endocrinol 15: 701-712

Lee SX, Heine M, Schlein C, Ramakrishnan R, Liu J, Belnavis G, Haimi I, Fischer AW, Ginsberg HN, Heeren J, Rinninger F, and Haeusler RA. (2018) FoxO Transcription Factors are Required for Hepatic HDL-Cholesterol Clearance J Clin Invest 128: 1615-1626

Kim KJ, Goldberg IJ, Graham MJ, Sundaram M, Bertaggia E, Lee SX, Qiang L, Haeusler RA, Metzger D, Chambon P, Yao Z, Ginsberg HN, and Pajvani UB (2018) Gamma-secretase inhibition lowers plasma triglyceride-rich lipoproteins by stabilizing the LDL receptor Cell Metab 27: 816-827

Bertaggia E, Jensen K, Castro-Perez J, Xu Y, Di Paolo G, Chan RB, Wang L, Haeusler RA. (2017) Cyp8b1 ablation prevents western diet-induced weight gain and hepatic steatosis due to impaired fat absorption. Am J Physiol Endocrinol Metab 313: E121-E133

Langlet, Haeusler RA, Linden D, Ericson E, Norris T, Johansson A, Cook JR, Aizawa K, Sang L, Buettner C, Accili D. (2017) Selective Inhibition of FOXO1 Activator/Repressor Balance Modulates Hepatic Glucose Handling. Cell 171:824-833

Haeusler RA, McGraw T, and Accili D. (2017) Biochemical and cellular properties of insulin receptor signaling. Nat Rev Mol Cell Biol. 19:31-44

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