Faculty

Brian Finck, Ph.D.
Research Assistant Professor in Medicine

Research Interests

The research conducted in Dr. Finck’s laboratory examines the molecular control of fatty acid metabolism with special emphasis on obesity-related abnormalities in liver, heart, and skeletal muscle lipid metabolism. Dr. Finck is particularly interested in the role that nuclear receptor transcription factors and associated proteins play in regulating these metabolic pathways. To this end, Dr. Finck’s lab employs a variety of techniques including molecular biological approaches, gene expression profiling (microarray), cell culture-based systems, and transgenic mouse models. Given the emerging epidemic of obesity, the long-term goal of these studies is to identify novel therapeutic target pathways for treatment of obesity-related diseases including diabetes, cardiovascular disease, and fatty liver disease.

Contact Information

Washington University School of Medicine
Division of Geriatrics and Nutritional Science
660 S. Euclid Avenue, Box 8031
St. Louis, MO 63110
Phone: (314) 362-8963
email: bfinck@dom.wustl.edu

Publications

Select Recent Publications:

1) Finck BN, Lehman JJ, Leone TC, Welch MJ, Bennett MJ, Kovacs A, Han X, Gross RW, Kozak R, Lopaschuk GD, and Kelly DP. 2002. The cardiac phenotype induced by PPARα overexpression mimics that caused by diabetes mellitus. J. Clin. Invest. 109:121-130.

2) Finck BN, Han X, Courtois M, Aimond F, Nerbonne JM, Kovacs A, Gross RW, and Kelly DP. 2003. A critical role for PPARα-mediated lipotoxicity in the pathogenesis of diabetic cardiomyopathy: Modulation by dietary fat content. Proc. Natl. Acad. Sci. USA 100:1226-1231.

3) Bernal-Mizrachi C, Weng S, Feng C, Finck BN, Knutsen RH, Leone TC, Coleman T, Mecham RP, Kelly DP, and Semenkovich CF. 2003. Glucocorticoid induction of hypertension and diabetes is PPARα-dependent in mice. Nat. Med. 9:1069-1075.

4) Finck BN, Bernal-Mizrachi C, Han DH, Coleman T, Sambandam N, LaRiviere LL, Holloszy JO, Semenkovich CF, and Kelly DP. 2005. A potential link between muscle peroxisome proliferator-activated receptor α signaling and obesity-induced insulin resistance. Cell Metab. 1:133-144.

5) Burgess SC, Leone TC, Wende AR, Croce MA, Chen Z, Sherry AD, Malloy CR, and Finck BN. 2006. Diminished hepatic gluconeogenesis via defects in tricarboxylic acid cycle flux in peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α)-deficient mice. J. Biol. Chem. 281: 19000-19008.

6) Finck BN and Kelly DP. 2006. PGC-1 Coactivators: Inducible Regulators of Energy Metabolism in Health and Disease. J. Clin. Invest. 116:615-622. (Review)

7) Finck BN, Gropler MC, Chen Z, Leone TC, Croce MA, Harris TE, Lawrence JC, and Kelly DP. 2006. Lipin 1 is an inducible amplifier of the hepatic PGC-1α / PPARα regulatory pathway. Cell Metab. 4: 199-210.

8) Croce MA, Eagon CJ, LaRiviere LL, Korenblat KM, Klein S, and Finck BN. 2007. Hepatic lipin 1ß expression is diminished in insulin-resistant obese subjects and is reactivated by marked weight loss. Diabetes. 56: 2395-2399.

Department of Medicine
Division of Geriatrics & Nutritional Sciences