Ron F. Morrison, Ph.D.
Instances of childhood obesity are rapidly rising in the United States. Considering the devastating long-term health implications associated with the onset of obesity at an early age, it is critically important to gain greater knowledge of the molecular mechanisms regulating the development of obesity in children.
Obesity occurs in two forms: hypertrophic obesity, or the excessive accumulation of fat tissue resulting from enlargement of existing adipocytes or "fat cells", and hyperplastic obesity, or the development of new adipocytes resulting from replication and subsequent differentiation of underveloped fat cells, or preadiopocytes. While both forms of obesity occur throughout lifem, it is primarily hyperplastic obesity and the development of new adipocytes that characterizes childhood obesity.
With extramural funding from the American Heart Association and the National Institutes of Health, Dr. Morrison investigates mechanisms of hyperplastic obesity using various cell culture models. His research is studying how undeveloped fat cels replicate and then how these new preadipocytes enter a process of differentiation where thousands of genes are activated or inhibited to produce mature adipocytes. It is expected that greater knowledge of these mechanisms will lead to future drugs or nutritional and behavioral therapies designed to prevent the development of obesity in our children.
Education- Ph.D., Physiology, East Carolina Univ. School of Medicine, 1994
- B.S., Biology, East Carolina University, 1978
Research Interest- Molecular mechanisms regulating adipocyte growth and differentiation; OBESITY
- Mechanisms linking obesity and insulin-resistance; DIABETES
Our research investigates cellular and molecular mechanisms of obesity and obesity-related diseases. Studies are conducted to better understand processes regulating adipocyte hyperplasia which is particularly important in the development of childhood obesity, as well as mechanisms that couple the onset of obesity and the rising incidence of diabetes.
- Nam H, Ferguson BS, Stephens JM, Morrison RF. (2013) Impact of obesity on IL-12 family gene expression in insulin responsive tissues. Biochem Biophys Acta. 1832(1):11-19.
- Ferguson BS, Nam H, Hopkins RG, Morrison RF. (2010) Impact of reference gene selection for target gene normalization on experimental outcome using real-time qRT-PCR in adipocytes.PLoS ONE 5(12): e15208. doi:10.1371/journal.pone.0015208.
- Fernandes KM, Auld CA, Hopkins RG, Morrison RF. (2008) Helenalin-mediated post-transcriptional regulation of p21(Cip1) inhibits 3T3-L1 preadipocyte proliferation. J Cell Biochem. 105(3):913-21.
- Consitt LA, Wideman L, Hickey MS, Morrison RF. (2008) Phosphorylation of the JAK2-STAT5 pathway in response to acute aerobic exercise. Med Sci Sports Exerc. 40(6):1031-1038.
- Auld CA, Fernandes KM, Morrison RF. (2007) Skp2-mediated p27(Kip1) degradation during S/G2 phase progression of adipocyte hyperplasia. J Cell Physiol. 211(1):101-111.
- Auld CA, Caccia CD, Morrison RF. (2007) Hormonal induction of adipogenesis induces Skp2 expression through PI3K and MAPK pathways. J Cell Biochem. 100(1):204-216.
- Auld CA, Hopkins RG, Fernandes KM, Morrison RF. (2006) Novel effect of Helenalin on Akt signaling and Skp2 expression in 3T3-L1 preadipocytes. Biochem Biophys Res Comm. 346(1):314-20.
- Auld CA, Morrison RF. (2006) Evidence for cytosolic p27(Kip1) ubiquitylation and degradation during adipocyte hyperplasia. Obesity 14(12):2136-2144.