Dr. Sean Limesand
Assistant Professor
Shantz Bldg 231
Phone: (520) 626-8903
E-Mail: limesand@ag.arizona.edu
Degrees
- Ph.D., Colorado State University
- M.S. Colorado State University
- B.S. North Dakota State University
Classes Taught:
- ANS 587 - Molecular Endocrinolgy
Dr. Sean Limesand is joined the Animal Sciences Department in 2005. Prior to joining U of A 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
- Rozance PJ, Limesand SW, Hay Jr WW. Mar 2006. Decreased Nutrient Stimulated Insulin Secretion in Chronically Hypoglycemic Late Gestation Fetal Sheep is Due to an Intrinsic Islet Defect. Am J Physiol Endocrinol Metab,2006 Mar 28;
- Wallace JM, Regnault TR, Limesand SW, Hay WW Jr, Anthony RV. May 2005. Investigating the causes of low birth weight in contrasting ovine paradigms. J Physiol, 565:19-26
- Limesand SW, Jensen J, Hutton JC, Hay WW Jr. May 2005. Diminished beta-cell replication contributes to reduced beta-cell mass in fetal sheep with intrauterine growth restriction. Am J Physiol Regul Integr Comp Physiol, 288:R1297-305
- Limesand SW, Rozance PJ, Zerbe GO, Hutton JC, Hay WW Jr. Dec 2005. Attenuated Insulin Release and Storage in Fetal Sheep Pancreatic Islets with Intrauterine Growth Restriction. Endocrinology,2005 Dec 8;
Limesand Lab
- Miranda Anderson - Research Specialist
- Rafael Leos - Research tech
- Lori Cole - Masters Student in Physiological Sciences
Animal Research Center
4101 N. Campbell Ave.
Phone 520-795-1592
