Chi Ma,1 Lance G. A. Nunes,2 Daniel J. Torres,3 FuKun W. Hoffmann,1 Peter R. Hoffmann,1 Matthew W. Pitts1
1 Department of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawaiʻi
2 Department of Anatomy, Biochemistry and Physiology, John A. Burns School of Medicine, University of Hawaiʻi
3 Pacific Biosciences Research Center, University of Hawaiʻi
Selenoprotein I (SELENOI) is a phosphotransferase that catalyzes the transfer of the ethanolamine phosphate group from CDP-ethanolamine to lipid donors, generating ethanolamine phospholipids. To investigate the special role of SELENOI in the central nervous system (CNS), we recently developed a unique CNS-specific SELENOI knockout (KO) mouse model by breeding Tuba1a-Cre mice with Selenoi Fl/Fl mice.
Beyond the neurological changes, the KO mice also display significantly reduced body weight.
To further evaluate their metabolic phenotype, we utilized a Bio-Plex Pro™ Mouse Assay to measure levels of Ghrelin, GIP, GLP-1, PAI-1, Glucagon, Insulin, Leptin, and Resistin in serum. Additionally, we used a metabolic measurement system to assess oxygen consumption and CO2 production, energy expenditure and food intake during both light and dark cycles.
Our results indicate that CNS-specific SELENOI KO mice exhibited decreased circulating leptin and increased Ghrelin levels. They also showed elevated energy expenditure, with higher oxygen consumption and CO₂ production compared to control mice. Meanwhile, KO mice display reduced food intake during the dark cycle, their active feeding period.
