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Selenium Protects Mouse Hypothalamic Cells from Glucocorticoid-Induced Endoplasmic Reticulum Stress Vulnerability and
Katlyn J An1, Ashley N Hanato1, Katherine W Hui1
1Department of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawai'i, Honolulu, HI 96813, USA.
Selenium protects the hypothalamus from glucocorticoid-induced metabolic dysfunction. Supplementing with selenium alleviates endoplasmic reticulum stress and improves insulin signaling, countering negative effects of corticosterone.
Area of Science:
- Endocrinology
- Neuroscience
- Nutritional Science
Background:
- Glucocorticoids induce metabolic side effects like weight gain and insulin resistance.
- The hypothalamus regulates energy balance and is sensitive to glucocorticoids.
- Glucocorticoids can increase oxidative stress and endoplasmic reticulum stress.
Purpose of the Study:
- To investigate selenium's protective role against glucocorticoid-induced hypothalamic dysfunction.
- To determine if selenium can mitigate corticosterone's negative effects on hypothalamic cells.
Main Methods:
- Mouse hypothalamic cells (mHypoE-44) were treated with corticosterone.
- Cellular physiology, endoplasmic reticulum stress, and insulin signaling were analyzed.
- The effects of selenium supplementation were assessed.
Main Results:
- Corticosterone exposure increased vulnerability to endoplasmic reticulum stress and impaired insulin signaling.
- Selenium supplementation reduced endoplasmic reticulum stress.
- Selenium promoted insulin signaling in the presence of corticosterone.
Conclusions:
- Selenium plays a protective role against chronic glucocorticoid-induced hypothalamic dysfunction.
- Selenium may be a therapeutic target for managing metabolic disorders associated with glucocorticoid use.
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