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.
View All Publications
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 is interested in genotype/phenotype relationships relevant to metabolic diseases, especially those involving fatty acid metabolism. We are 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 focuses on two major areas:
Philip Wood's Research Report
The Wood Lab is interested in genotype/phenotype relationships regarding
metabolic diseases, especially those involving fatty acid metabolism. This
includes rare inherited enzyme deficiencies that affected primarily children, as
well as more common diseases or processes that include obesity-related traits.
These include insulin resistance, fatty liver disease, metabolic syndrome and
type 2 diabetes mellitus. This approach allows us to identify genes (genotype)
that help explain the basic cause of disease traits (phenotype). Furthermore,
this information often points us toward disease mechanisms and potential new
We are interested in understanding what versions (alleles) of genes in
individuals that may cause, predispose, or protect them from disease traits
during conditions of excess fat.
In order to understand the genetic and metabolic mechanisms underlying these
diseases, we've developed mouse models of these diseases via gene targeting of
mouse embryonic stem cells resulting in “knocking out” six different enzymatic
steps in this pathway. These steps include carnitine palmitoyltransferase-1a and
1b (liver and muscle isoforms), very long-chain, long-chain, medium-chain and
short-chain acyl-CoA dehydrogenases. We also have an active pediatric patient
protocol at Florida Hospital Pediatric Endocrinology and Metabolism Clinic and
the Translational Research Institute for Metabolism and Diabetes to study
patients and their family members with these rare inherited diseases.
Our studies can be summarized in two major areas:
Ongoing and evolving research projects include:
- 1. Inherited enzyme deficiencies in the mitochondrial fatty acid
These disorders primarily affect children and are characterized by
phenotypes that include poor fasting tolerance, sudden infant death, fatty
liver, and heart diseases.
- 2. Obesity-related disease traits that include fatty liver, insulin
resistance, pro-inflammatory state, metabolic syndrome, pancreatic beta-cell
loss and development of type 2 diabetes.
This is a problem of having a genotype that predisposes individuals to these
problems in the face of obesity. Thus, this is a genetics of predisposition,
poor response or intolerance of the extra fat load provided by obesity.
There are also those who, despite their obesity, do not develop these
secondary disease processes and that would represent having a genetics of
resistance to the excess fat of obesity. Both scenarios are of great
Inborn errors of mitochondrial fatty acid oxidation. The study in our mouse models of double heterozygosity for fatty acid oxidation enzyme deficiencies in a process we have called synergistic heterozygosity. This is an important concept that may be useful to investigate multigene interactions in more common diseases with genetic components such as obesity and type 2 diabetes.
- 2. Genetic and metabolic bases of obesity-related diseases and disease processes. Developing a mouse model of metabolic syndrome based on synergistic heterozygosity to model multigene interactions. This will allow us to quantify gene interactions, as well as dissect the many obesity related components of metabolic syndrome.
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