Brian Finck, Ph.D.
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.
Washington University School of Medicine
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 PPAR-alpha 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 PPAR-alpha-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 PPAR-alpha-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 alpha 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 alpha 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 / PPAR-alpha 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.
9) Chen Z, Gropler MA, Norris J, Lawrence JC, Harris TE, and Finck BN. 2008. Alterations in hepatic metabolism in fld mice reveal a role for lipin 1 in regulating VLDL-triacylglyceride metabolism. Arterioscler. Thromb. Vasc. Biol. 28:1738-1744.
10) Gropler MC, Hall AM, Han X, Gross RW, Harris TE, Chen Z, and Finck BN. 2009. Lipin 2 is a liver-enriched phosphatidate phosphohydrolase enzyme that is dynamically regulated by fasting and obesity in mice. J. Biol. Chem. 284:6763-6772.
Department of Medicine