The University of Arizona
Dr. Sean Limesand

Dr. Sean Limesand

Associate Professor

Agricultural Research Center
4101 North Campbell Ave
Tucson, AZ 85719
Phone: (520) 626-8903
Fax: (520) 626-1283
E-Mail: limesand@ag.arizona.edu

Degrees

Classes Taught:

Dr. Sean Limesand joined the Animal Sciences Department in 2005. Prior to joining the UA he worked at the University of Colorado Health Sciences Center as a Postdoctoral Fellow in the Department of Pediatrics and later as an Instructor in the Department of Pediatrics. Dr. Limesand's graduate studies focused mainly on fetal growth and development in sheep, specifically how abnormal fetal nutrition influences the formation and function of the pancreas. He continues his study of the endocrine system and Type 2 Diabetes at the U of A, primarily through sheep trials.

Research Interests

Some of the most debilitating diseases affecting public health and those that impose an extreme monetary impact on health care costs in the United States are metabolic diseases and endocrine disorders such as Type 2 Diabetes. The prevalence of these diseases in the USA has been growing faster than Mendelian inheritance rates suggesting that environmental cues are influencing the prevalence of adulthood metabolic disorders. Inappropriate fetal growth and development due to inadequate fetal nutrition has been associated with several adult onset diseases including diabetes (Barker Hypothesis). Pancreatic b-cells secrete the anabolic hormone, insulin, in response to nutrient changes during the second half of gestation, likely coordinating fetal growth rate with fetal nutrient supply, making the fetal b-cell a potential target for nutritional adaptation in utero.

To understand nutrient regulation of fetal pancreas development, I am studying how poor fetal nutrition reduces pancreas formation and function. Environmental stress during pregnancy in sheep causes placental insufficiency; thus, creating an inadequate fetal nutrient supply that leads to fetal growth restriction and impaired insulin secretion due to decreased b-cell number and function. Current research aims are designed to determine mechanism that reduced cell responsiveness in intrauterine growth restricted fetuses.

The first aim is to determine stages of pancreatic development and endocrine cell replication in this large animal model to understand how b-cell numbers are reduced. In addition to a lower number of cells, their stimulus secretion coupling is impaired due to reduced insulin production. Therefore, the second aim is to determine deficits in insulin biosynthesis. If these inadequacies shown in the growth restricted fetus are not compensated for after birth, they might persist into adulthood and contribute tofailure of insulin secretion to predispose offspring to Type 2 Diabetes.

Selected Publications

Limesand Lab

Animal Research Center
4101 N. Campbell Ave.
Phone 520-795-1592

to top