Knockout of Gpx1 exerted differential impacts on responses of lipid‐metabolism related genes to high dietary Se intake between liver and adipose tissue

Abstract

This study was conducted to explore molecular mechanisms for our previously-observed impacts of a moderately high Se (1.0 vs. 0.3 mg/kg as selenite) and (or) high fat (30 vs. 5% as lard) diets on the liver and adipose tissue lipid profiles of wild-type (WT) and Gpx1-/-male mice at 2 ages (young adult, 2-4 mo) and old (6-10 mo). The liver and adipose tissue samples were collected from the previous experiment (total = 80 mice, n = 5/diet by age and genotype) and assayed for responses of lipid metabolism-related genes. In the WT adipose tissue, the high Se diet down-regulated (P < 0.05) a number of genes involved in pathways of cell proliferation, mitochondrial biogenesis, and cell-cell interactions, but up-regulated (P < 0.05) 2 genes in the cell cycle pathway (Klhdc3 and Ccng1). In contrast, the impacts of the high Se diet on these genes in the WT liver were essentially opposite to those in the WT adipose tissue. While the Gpx1 knockout blocked all the impacts of the high Se diet on these genes in the liver, the Gpx1-/- adipose tissue showed responses to the high Se diet similar to those of the WT adipose tissue. While comparing responses of the WT tissues to the high Se and high fat diets might help reveal candidate genes responsible for the diabetogenic effects of the high Se intake, knockout of Gpx1 seemed to exert differential impacts on those responses between the liver and adipose tissue (NIH DK 53018).