Normal AT remodeling requires a balance between the synthesis and degradation of a complex network of extracellular matrix (ECM) proteins. Disruption of this balance, as observed in obesity, can lead to AT fibrosis and inflammation. We have reported that oncostatin M (OSM), a gp130 cytokine, is produced by AT macrophages and up-regulated in mouse and human obesity. Our data demonstrate that adipocyte-specific knockout of the OSM-specific receptor (OSMR) in mice leads to insulin resistance, glucose intolerance, and increased pro-fibrotic and pro-inflammatory gene expression in visceral AT. The proposed aims will test the overall hypothesis that that loss of adipocyte OSMR signaling disrupts normal adipose tissue homeostasis and promotes AT fibrosis and insulin resistance. Importantly, Dr. Elks will learn and implement new methods in transgenic mouse generation and phenotyping, molecular biology, and the biochemical assessment and imaging of the AT-ECM that are necessary for her independence as an investigator. Pennington Biomedical Research Center will provide an ideal learning environment for Dr. Elks to successfully complete the proposed aims and objectives. The training in this research project will also provide a basis for future projects to assess alterations in AT-ECM biology and adipocyte metabolism in metabolic diseases, and to apply findings to the development of novel therapies for insulin resistance and obesity, which is Dr. Elks' long-term research goal. The PI has assembled an outstanding mentoring team of experienced investigators and collaborators who will all provide their guidance and expertise to help her achieve independence.

Public Health Relevance

Obesity, defined as fat (adipose) tissue excess, is a primary contributor to type 2 diabetes and a major healthcare burden. As obesity develops, adipose tissue becomes dysfunctional and often leads to additional metabolically unfavorable effects. The proposed research is relevant to public health because it will: 1) examine novel factors regulating adipose tissue function, and 2) provide understanding on how these factors can contribute to metabolic disorders

National Institute of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Research Scientist Development Award - Research & Training (K01)
Project #
Application #
Study Section
Kidney, Urologic and Hematologic Diseases D Subcommittee (DDK)
Program Officer
Spain, Lisa M
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Lsu Pennington Biomedical Research Center
Organized Research Units
Baton Rouge
United States
Zip Code
Stephens, Jacqueline M; Bailey, Jennifer L; Hang, Hardy et al. (2018) Adipose Tissue Dysfunction Occurs Independently of Obesity in Adipocyte-Specific Oncostatin Receptor Knockout Mice. Obesity (Silver Spring) 26:1439-1447
Turner, Paul A; Gurumurthy, Bhuvaneswari; Bailey, Jennifer L et al. (2017) Adipogenic Differentiation of Human Adipose-Derived Stem Cells Grown as Spheroids. Process Biochem 59:312-320
Warfel, Jaycob D; Vandanmagsar, Bolormaa; Dubuisson, Olga S et al. (2017) Examination of carnitine palmitoyltransferase 1 abundance in white adipose tissue: implications in obesity research. Am J Physiol Regul Integr Comp Physiol 312:R816-R820
Warfel, Jaycob D; Bermudez, Estrellita M; Mendoza, Tamra M et al. (2016) Mitochondrial fat oxidation is essential for lipid-induced inflammation in skeletal muscle in mice. Sci Rep 6:37941