(OR09-03-24) Thyroid Hormone Status in Mice Lacking Selenium Recycling

Sunday, June 30, 2024

8:24 AM – 8:36 AM CT

Location: W375A

Presenting Author(s)

Lucia A. Seale, PhD (she/her/hers)

Associate Researcher
University of Hawai'i
Honolulu, Hawaii, United States

Disclosure(s): No relevant financial relationship(s) with ineligible companies to disclose.

Co-Author(s)

PS

Princess J. Santiago

University of Hawai'i, Hawaii, United States
NA

Naghum Alfulaij

University of Hawaii at Manoa
SS

Sydonie Swanson

University of Hawaii at Manoa
PT

Pamela Toh

Icahn School of Medicine at Mount Sinai, New York, United States
Briana K. Shimada, PhD

Assistant Researcher
University of Hawaii at Manoa
Honolulu, Hawaii, United States

Objectives: Selenium (Se) recycling in cells is carried out by the enzyme selenocysteine (Sec) lyase (Scly), which decomposes the amino acid Sec to provide Se back to selenoprotein synthesis. Mice without Scly (Scly KO) reduce their thermogenic capacity in the brown adipose tissue (BAT), leading to obesity. Thermogenesis is critically regulated by thyroid hormone (TH) status and activation by the enzyme type 2 deiodinase (Dio2) in brown adipocytes (BA). Thus, our objective is to evaluate circulating TH levels and activation in Scly KO mice and mice lacking Scly in BA only (BA-Scly KO).

Methods: Wild-type (WT), floxed control (C), Scly KO, and BA-Scly KO mice were fed customized low (0.08 ppm) or adequate (0.2 ppm) Se diets for 8 weeks after weaning. Thyroid status was determined in serum by assessing total T3 and T4 by ELISA, and TSH levels by Luminex using commercial kits. Dio2 expression was measured by qPCR with specific primers.

Results: Scly KO mice had elevated TSH levels, but T3 and T4 were only affected by dietary Se. Downregulation of Dio2 occurred when Scly KO mice were fed a Se-deficient diet. BA-Scly KO mice thyroid status was normal compared to C, while Dio2 was downregulated in mice BA.

Conclusions: Se recycling modulates thyroid hormone activation and, consequently, thermogenic capacity in mice.

Funding Sources: National Institute of Diabetes and Digestive and Kidney Diseases; National Institute of General Medical Sciences; Hawaii Community Foundation