Are Hypothyroidism-Induced Reductions in Brain Derived Igf1 Due to Reductions in Serum Growth Hormone?
Location
CSU Ballroom
Start Date
11-4-2017 10:00 AM
End Date
11-4-2017 11:30 AM
Student's Major
Biological Sciences
Student's College
Science, Engineering and Technology
Mentor's Name
David Sharlin
Mentor's Department
Biological Sciences
Mentor's College
Science, Engineering and Technology
Description
Low thyroid hormone (TH) during development results in permanent neurological deficits. Similarly, low insulin-like growth factor 1 (Igf1) during development results in neurological deficits. Furthermore, studies in rodents have documented similar neuroanatomical defects between low serum TH and low serum Igf1. Serum Igf1 levels are controlled by pituitary-derived GH that stimulates the production and secretion of Igf1 from the liver. Considering that TH is well known to regulate pituitary derived GH production, it is reasonable to propose that changes in locally produced brain-derived Igf1 following thyroid hormone insufficiency is due, in part, to a disruption of the TH-GH-Igf1 axis. To clarify this, we are investigating whether changes in brain-derived Igf1 mRNA is an indirect result of changes in serum GH that accompany low TH. To test this idea, pups derived from control or hypothyroid timed-pregnant dams are injected daily with 15ng/day of GH or saline for 7 days post birth and then 30ng/day for the following 7 days post birth. On postnatal day 14 (P14), brains were dissected and blood serum was collected. Using enzyme-linked immunosorbent assays (ELISA) serum GH and Igf1 are being determined and compared between groups. Using quantitative real-time PCR (qRT-PCR) brain derived Igf1 mRNA will be determined in known TH-responsive brain regions. It is predicted that these data will demonstrate that changes in brain-derived Igf1 levels following hypothyroidism are independent of the reductions in serum growth hormone associated with low TH; identifying a potentially novel process by which low TH in development results in neuroanatomical defects.
Are Hypothyroidism-Induced Reductions in Brain Derived Igf1 Due to Reductions in Serum Growth Hormone?
CSU Ballroom
Low thyroid hormone (TH) during development results in permanent neurological deficits. Similarly, low insulin-like growth factor 1 (Igf1) during development results in neurological deficits. Furthermore, studies in rodents have documented similar neuroanatomical defects between low serum TH and low serum Igf1. Serum Igf1 levels are controlled by pituitary-derived GH that stimulates the production and secretion of Igf1 from the liver. Considering that TH is well known to regulate pituitary derived GH production, it is reasonable to propose that changes in locally produced brain-derived Igf1 following thyroid hormone insufficiency is due, in part, to a disruption of the TH-GH-Igf1 axis. To clarify this, we are investigating whether changes in brain-derived Igf1 mRNA is an indirect result of changes in serum GH that accompany low TH. To test this idea, pups derived from control or hypothyroid timed-pregnant dams are injected daily with 15ng/day of GH or saline for 7 days post birth and then 30ng/day for the following 7 days post birth. On postnatal day 14 (P14), brains were dissected and blood serum was collected. Using enzyme-linked immunosorbent assays (ELISA) serum GH and Igf1 are being determined and compared between groups. Using quantitative real-time PCR (qRT-PCR) brain derived Igf1 mRNA will be determined in known TH-responsive brain regions. It is predicted that these data will demonstrate that changes in brain-derived Igf1 levels following hypothyroidism are independent of the reductions in serum growth hormone associated with low TH; identifying a potentially novel process by which low TH in development results in neuroanatomical defects.
Recommended Citation
Wright, Alec. "Are Hypothyroidism-Induced Reductions in Brain Derived Igf1 Due to Reductions in Serum Growth Hormone?." Undergraduate Research Symposium, Mankato, MN, April 11, 2017.
https://cornerstone.lib.mnsu.edu/urs/2017/poster-session-A/23
