I have had a long term interest in the role of mitochondrial fatty acid oxidation (FAO) in disease processes. This includes both genetic and nutritional determinants of rare inherited FAO enzyme deficiencies, as well as the body’s mechanisms of handling excess fat in obesity.
Dr. Wood investigates the role of abnormal fatty acid metabolism in rare inherited diseases and obesity-related disorders.
Dr. Wood received his DVM and MS degrees from Kansas State University in 1980 and his PhD from University of Alabama at Birmingham in 1983.
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Genomic structure and genetic drift in C57BL/6 congenic metabolic mutant mice.
Almodovar AJ, Luther RJ, Stonebrook CL, Wood PA
Mol Genet Metab. 2013 Nov;110(3):396-400
Carnitine palmitoyltransferase-1b deficiency aggravates pressure overload-induced cardiac hypertrophy caused by lipotoxicity.
He L, Kim T, Long Q, Liu J, Wang P, Zhou Y, Ding Y, Prasain J, Wood PA, Yang Q
Circulation. 2012 Oct 2;126(14):1705-16
Long term effects of high fat or high carbohydrate diets on glucose tolerance in mice with heterozygous carnitine palmitoyltransferase-1a (CPT-1a) deficiency: Diet influences on CPT1a deficient mice.
Nyman LR, Tian L, Hamm DA, Schoeb TR, Gower BA, Nagy TR, Wood PA
Nutr Diabetes. 2011 Aug 22;1:e14
Resistance to high-fat diet-induced obesity and insulin resistance in mice with very long-chain acyl-CoA dehydrogenase deficiency.
Zhang D, Christianson J, Liu ZX, Tian L, Choi CS, Neschen S, Dong J, Wood PA, Shulman GI
Cell Metab. 2010 May 5;11(5):402-11
Cardiac hypertrophy in mice with long-chain acyl-CoA dehydrogenase or very long-chain acyl-CoA dehydrogenase deficiency.
Cox KB, Liu J, Tian L, Barnes S, Yang Q, Wood PA
Lab Invest. 2009 Dec;89(12):1348-54
Philip Wood's Research Focus
Metabolic Diseases, Obesity, Type 2 Diabetes
Watch Dr. Wood describe
The Wood lab has been interested in genotype/phenotype relationships relevant to metabolic diseases, especially those involving fatty acid metabolism. We were interested in what alleles (versions) of genes that be a primary cause of diseases such as rare inherited enzyme deficiencies affecting children to versions of genes that predispose or even protect individuals from the problems often associated with excess fat presented to the body in obese states. 1. Inherited enzyme deficiencies in the mitochondrial fatty acid oxidation pathway.
2. Obesity-related disease traits that include fatty liver, pro-inflammatory state, insulin resistance and the many traits associated with metabolic syndrome.
Using six mouse models and now human patients with rare inherited enzyme deficiencies of the fat burning pathway, our research was focused on two major areas:
About Philip Wood
Philip A. Wood, D.V.M, Ph.D., was born in Eldorado, Illinois, in 1956 and subsequently grew up in Kansas. In 1980 he received his Doctor of Veterinary Medicine and Master of Science degrees from Kansas State University and in 1983 received his Doctor of Philosophy in Experimental Pathology from the University of Alabama at Birmingham (UAB). From 1983-1988 he was on the faculty in the Institute for Molecular Genetics at Baylor College of Medicine in Houston, Texas. In 1989, Dr. Wood returned to UAB as an Associate Professor. He was appointed as a Professor in 1996, and served as Chairman of the UAB Department of Genomics and Pathobiology from 1996-2002. Dr. Wood was Professor and Director of the Division of Genomics in the UAB Department of Genetics through 2007, and finally Professor in 2008.
In January 2009, Dr. Wood was appointed Professor at Sanford-Burnham Medical Research Institute at Lake Nona where he works on the role of genetics and fat metabolism in rare inherited metabolic diseases, as well as obesity–related disease processes such as insulin resistance, metabolic syndrome, and type 2 diabetes. He recently published the book How Fat Works (Harvard University Press, 2006).
Volunteer Professor at the University of Central Florida and the University of Florida