Philip Wood

Philip Wood, D.V.M., Ph.D.[Lake Nona in Orlando]

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.

  • Research

    Dr. Wood investigates the role of abnormal fatty acid metabolism in rare inherited diseases and obesity-related disorders.

  • Biography

    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.

Philip Wood's Research Focus

Metabolic Diseases, Obesity, Type 2 Diabetes

Philip WoodWatch Dr. Wood describe
his research

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.

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:

  • 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.
  • Philip Wood's Research Report

    Philip Wood
    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 drug targets. 

    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:

    1. 1. Inherited enzyme deficiencies in the mitochondrial fatty acid oxidation pathway. These disorders primarily affect children and are characterized by phenotypes that include poor fasting tolerance, sudden infant death, fatty liver, and heart diseases.

    2. 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 interest.

    Ongoing and evolving research projects include:

    • 1. 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).

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