The University of Arizona

Effects of environmental stress and chronic malnutrition on fetal growth and development.

-Dr. Sean Limesand, Ph.D.

Pregnant ewes exposed to enviromental heat stress give birth to small offspring due to placental insufficiency that lowers the fetal nutrient supply and leads to intrauterine growth restriction (IUGR). Dr. Limesand's research is on fetal growth and development with an emphasis on how the fetus adapts to chronic undernutrition. In the fetus pancreatic β-cells release insulin in response to nutrients like glucose to promote nutrient utilization and fetal growth. Adaptations in the endocrine pancreas play an important role in coordinating the rate of fetal growth to the fetal nutrient supply. Therefore, in chronic abnormal nutrient conditions can impact endocrine pancreas development by altering its cellular distribution or function by impairing insulin secretion to allow the fetus to survive. After birth, the pancreatic endocrine cells maintain glucose homeostasis; therefore, if deficits from fetal life persist they might lead to postnatal complications in animal growth and lower profits for livestock producers.

In the IUGR fetuses from our heat stress ewes, we have shown lower insulin secretion by mid-gestation and the disparity continues to increase between normal and IUGR fetuses until term. We find that the IUGR fetal pancreas contains lower numbers of β-cells and that these β-cells are unable to make adequate amounts of insulin. We also found that the IUGR fetal β-cells are unable to increase oxidative glucose metabolism in response to increasing glucose concentrations. Since signals derived from the oxidative metabolism of glucose are implicated in the regulation of insulin release and insulin production, a defect in the β-cell's ability to increase oxidative metabolism in response to an increase in extracellular glucose concentration has major implications in terms of b-cell function. These results demonstrate that the fetal pancreas adapts to the low nutrient environment by altering its structure, physiology, and metabolism.

Prenatal adaptations are more than likely critical for fetal survival, but after birth these adjustments if they persist might create long term complications. The impact of the fetal pancreatic adaptations to nutrient deprivation can be divided into four areas influencing livestock production: (1) prenatal and perinatal death loss, (2) postnatal growth rates, (3) reproductive fecundity, and (4) carcass characteristics at slaughter. These areas may not be recognized until adulthood or remain as an unforeseen expense absorbed by livestock producers. Therefore, Dr. Limesand will continue to understand mechanisms responsible for nutrient induced pancreatic adaptations and whether these adaptations program the pancreas to lower postnatal performance in production animals.

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