Brian N. Finck, Ph.D.

Associate Professor
Internal Medicine
Geriatrics and Nutritional Sciences

Molecular Cell Biology Program

  • 314-362-8963

  • 314-362-8230

  • 1754 West Building



  • diabetes, fatty acid, insulin, cardiovascular disease, fatty liver disease, mitochondria

  • Identify novel target pathways for therapeutic treatment of obesity-related diseases including diabetes, cardiovascular disease, and fatty liver disease

Research Abstract:

My laboratory in the Division of Geriatrics and Nutritional Sciences at Washington University is focused on many aspects of lipid and glucose metabolism in insulin sensitive tissues, with special interest in the liver, and on understanding how these processes become deranged in obesity. In the course of these studies, we have become experts in a variety of areas of metabolism, including transcriptional regulation, lipid biochemistry, mitochondrial function and metabolism, and characterizing the metabolic status of mouse models. Current research projects in the lab are focused on enzymes that are involved in complex lipid synthesis as well as several projects on basic aspects of mitochondrial metabolism. We believe that these research efforts will provide important information about the regulation of basic aspects of intermediary metabolism and their impact on systemic homeostasis. The long term goal of these studies is to identify new sites for pharmaceutical intervention with the goal of targeting obesity-related metabolic disease.

Mentorship and Commitment to Diversity Statement:

I am originally from a small town in central Illinois and grew up on a farm. My parents were the first from their families to attend and graduate from college. While they may not have understood my need to obtain a graduate degree or work in academia, they instilled in me the value of education, hard work, and caring and kindness towards all.

My high school graduating class was composed of only 32 students. It was a very homogeneous culture; almost everyone was from that general area of Illinois originally and was of German ancestry. Though my upbringing lacked exposure to people from diverse backgrounds, my collegiate and professional experiences since then have been enriched by interacting with people who were raised in different environments and cultures. Over the years, my lab has welcomed trainees from around the world and I value the wonderful experiences I’ve had learning about their lives.

For the past several years, I have served on the Postdoctoral Research Advisory Committee, which is committed to enhancing diversity, equity, and inclusion at Washington University. I am also personally committed to these goals and to mentoring people from all backgrounds. I have mentored trainees from backgrounds that are underrepresented in the life sciences and I am committed to continuing efforts to address inequalities and representation in this field. I look forward to future opportunities to learn and grow in this area.

Selected Publications:

1) McCommis KM, Hodges WT, Bricker D, Wisidagama DR, Remedi MS, Thummel C, and Finck BN. 2016. An ancestral role for the mitochondrial pyruvate carrier in glucose-stimulated insulin secretion. Mol. Metab. 5:602-614.

2) McCommis KS, Chen Z, Fu X, McDonald WG, Colca JR, Kletzien RF, Burgess SC, and Finck BN. 2015. Loss of mitochondrial pyruvate carrier 2 in liver leads to defects in gluconeogenesis and compensation via pyruvate-alanine cycling. Cell Metabolism. 22:682-694.

3) Vigueira PA, McCommis KS, Schweitzer GG, Remedi MS, Chambers KT, Fu X, McDonald WC, Cole S, Colca JR, Kletzien RF, Burgess SC, and Finck BN. 2014. Mitochondrial pyruvate carrier 2 hypomorphism in mice leads to defects in glucose-stimulated insulin secretion. Cell Reports. 7:2042-2053.

4) Hall AM, Soufi N, Chambers KT, Chen Z, Schweitzer GG, McCommis KS, Erion DM, Graham MJ, Su X, and Finck BN. 2014. Abrogating monoacylglycerol acyltransferase activity in liver improves glucose tolerance and hepatic insulin signaling in obese mice. Diabetes. 63:2284-2296.

5) Chambers KT, Chen Z, Lai L, Leone TC, Towle HC, Kralli A, Crawford PA, and Finck BN. 2013. PGC-1 and ChREBP partner to cooperatively regulate hepatic lipogenesis in a glucose concentration-dependent manner. Mol. Metab. 2:194-204.

6) Mitra MS, Chen Z, Ren H, Harris TE, Chambers KT, Hall AM, Nadra K, Klein S, Chrast R, Su X, Morris AJ, and Finck BN. 2013. Mice with an adipocyte separation-of-function allele reveal unexpected roles for phosphatidic acid in metabolic regulation. Proc. Natl. Acad. Sci. USA. 110:642-647.

7) Chen Z, Vigueira PA, Chambers KT, Hall AM, Mitra MS, McDonald W, Colca J, Kletzien RF, and Finck BN. 2012. Hepatic insulin resistance and metabolic derangements in obese mice are ameliorated by a novel thiazolidinedione via PPAR-independent effects. J. Biol. Chem. 287:23537-23548.

8) Peterson TR, Sengupta SS, Harris TE, Laplante M, Yesilaltay A, Madden K, Carpenter AE, Finck BN, and Sabatini DM. 2011. mTORC1 regulates lipin 1 nuclear localization to control lamin A structure and the SREBP pathway. Cell. 146: 408-420.

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

10) 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-1/PPAR regulatory pathway. Cell Metab. 4: 199-210.

Last Updated: 3/25/2021 3:33:53 PM

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