School of Health and Human Sciences

Deborah E. Kipp

Deborah E. Kipp, Ph.D., R.D.N.
Emeritus Professor
Ph.D., Cornell University
Curriculum Vitae

Brief Bio

Dr. Debbie Kipp’s research focuses on the effects of nutritional and hormonal imbalances – particularly related to iron and prolactin – on bone formation and maintenance using animal models and cell culture models.

Iron deficiency anemia results in low bone mass and brittle bones in animal models. The reasons for this loss of bone is not known, although the lack of iron may prevent normal production of collagen, which forms the matrix that then gets mineralized to form the basic structure of bone. Low iron levels may also prevent normal bone formation by altering growth factors that are important for normal bone formation and turnover.

High iron levels may add oxidative stress to bone cells, thereby enhancing cell damage and death. Studies investigating these possible mechanisms of iron-related effects on bones are underway.

Research in hormonal imbalance focuses on prolactin secretion which increases with age and may be a contributor to bone loss and osteoporosis. Initial tests showed that older rats retained the bone mass of younger rats when the normal age-related increase in prolactin was prevented. This study has prompted investigations using bone cell models to study prolactin’s effect at the cellular level.

Dr. Kipp’s research has been funded by NIH, USDA, industry, and foundations.

Research Interests

The role of nutrients, bioactive food components, and hormones in regulating osteoblast function and bone remodeling, using animal models and cell culture.

Current Projects

  • Age-related prolactin effects on the skeleton.
  • Effects of iron imbalance on bone development.
  • Effects of bioactive food components on bone formation.

Selected Publications

  • Messer JG, La S, Hopkins RG, Kipp DE. Quercetin partially preserves development of osteoblast phenotype in fetal rat calvaria cells in an oxidative stress environment. J Cell Physiol 2016 Dec;231(12):2779-88.
  • Messer JG, Hopkins RG, Kipp, DE. Quercetin metabolites up-regulate the antioxidant response in osteoblasts isolated from fetal rat calvaria. J Cell Biochem 2015 Sept;116(9):1857-66.
  • Messer, J.G., Cooney, P.T., Kipp, D.E. Iron chelator deferoxamine alters iron-regulatory genes and proteins and suppresses osteoblast phenotype in fetal rat calvaria cells. Bone 2010;46(5):1408-15.
  • Messer, J.G., Kilbarger, A.K., Erikson, K.M., Kipp, D.E. Iron overload alters iron-regulatory genes and proteins, down-regulates osteoblastic phenotype, and is associated with apoptosis in fetal rat calvaria cultures. Bone 2009;45(5):972-9.
  • Kipp, D.E., Grey, C.E., McElvain, M.E., Kimmel, D.B., Robinson, R.G., and Lukert, B.P. Long-term low ascorbic acid intake reduces bone mass in guinea pigs. J. Nutr. 1996;126:2044-2049.
  • Kipp, D.E., McElvain, M., Kimmel, D.B., Akhter, M.P., Robinson, R.G. and Lukert, B.P. Scurvy results in decreased collagen synthesis and bone density in the guinea pig animal model. Bone 1996;18:281-8.
  • Pate, S.K., Lukert, B.P. and Kipp, D.E. Tissue vitamin C levels of guinea pig offspring are influenced by maternal vitamin C intake during pregnancy. J. Nutr. Biochem.1996;7:524-8.