Matthew S Rodeheffer PhD

Assistant Professor of Comparative Medicine and of Molecular, Cellular, and Developmental Biology

Research Interests

Genomics; Stem Cells


Research Summary


Obesity, which is defined as an excessive increase in white adipose tissue (fat) mass, is one of the leading public health concerns of the 21st century. The relevance of obesity as a public health concern is due to two main factors 1) the rates of obesity have increased over the last thirty years and today almost one third of the adult population in the U.S. is classified as obese, and 2) obesity is associated with several other health conditions, including type 2 diabetes, cardiovascular disease and some forms of cancer.

Despite the importance of fat in human disease our understanding of the regulation of fat mass is limited. The research in my laboratory is directed toward elucidating the molecular mechanisms that regulate fat mass and contribute to the development of obesity and obesity associated pathologies. Specifically, we focus on identifying and characterizing fat progenitor and stem cells and the molecular processes that control the differentiation of these cells into mature, lipid-filled fat cells.

We take several approaches to accomplish our research goals, employing several mouse models of human disease, human primary cell culture, genomic and proteomic techniques and developing novel mouse models for the study of fat regulation. Determining how the growth of fat is regulated may lead to the development of novel therapeutics for the treatment of obesity, diabetes and cardiovascular disease.

Extensive Research Description

Obesity, which is defined as an excessive increase in white adipose tissue (fat) mass, is one of the leading public health concerns of the 21st century. The relevance of obesity as a public health concern is due to two main factors 1) the rates of obesity have increased over the last thirty years and today almost one third of the adult population in the U.S. is classified as obese, and 2) obesity is associated with several other health conditions, including type 2 diabetes, cardiovascular disease and some forms of cancer.

Despite the importance of fat in human disease our understanding of the regulation of fat mass is limited. The research in my laboratory is directed toward elucidating the molecular mechanisms that regulate fat mass and contribute to the development of obesity and obesity associated pathologies. Specifically, we focus on identifying and characterizing fat progenitor and stem cells and the molecular processes that control the differentiation of these cells into mature, lipid-filled fat cells.

We take several approaches to accomplish our research goals, employing several mouse models of human disease, human primary cell culture, genomic and proteomic techniques and developing novel mouse models for the study of fat regulation. Determining how the growth of fat is regulated may lead to the development of novel therapeutics for the treatment of obesity, diabetes and cardiovascular disease.


Selected Publications

  • Rodeheffer MS, Birsoy K, Friedman JM. Identification of white adipocyte progenitor cells in vivo. (2008) Cell. 135(2):240-9.
  • Zeigerer A, Rodeheffer MS, McGraw TE, Friedman JM. Insulin regulates leptin secretion from 3T3-L1 adipocytes by a PI 3 kinase independent mechanism. (2008) Exp Cell Res. 314(11-12):2249-56.
  • Bonawitz ND, Rodeheffer MS, Shadel GS (2006) Defective mitochondrial gene expression results in reactive oxygen species-mediated inhibition of respiration and reduction of yeast life span. Mol Cell Biol. 26(13):4818-29.
  • Taylor SD, Zhang H, Eaton JS, Rodeheffer MS, Lebedeva MA, O'rourke TW, Siede W, Shadel GS (2005) The conserved Mec1/Rad53 nuclear checkpoint pathway regulates mitochondrial DNA copy number in Saccharomyces cerevisiae. Mol Biol Cell. 16(6):3010-8.
  • Rodeheffer MS, Shadel GS (2003) Multiple interactions involving the amino-terminal domain of yeast mtRNA polymerase determine the efficiency of mitochondrial protein synthesis. J Biol Chem. 278(20):18695-701.

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