Prolonged Dietary Selenium Deficiency or Excess Does Not Globally Affect Selenoprotein Gene Expression and/or Protein Production in Various Tissues of Pigs

Abstract

We previously determined the effects of dietary selenium (Se) deficiency or excess on mRNA abundance of 12 selenoprotein genes in pig tissues. In this study, we determined the effect of dietary Se on mRNA levels of the remaining porcine selenoprotein genes along with protein production of 4 selenoproteins (Gpx1, Sepp1, Selh, and Sels) and body glucose homeostasis. Weanling male pigs (n = 24) were fed a Se-deficient (<0.02 mg Se/kg), basal diet supplemented with 0, 0.3, or 3.0 mg Se/kg as Se-enriched yeast (Angel Yeast) for 16 wk. Although mRNA abundance of the 13 selenoproteins in 10 tissues responded to dietary Se in 3 patterns, there was no common regulation for any given gene across all tissues or for any given tissue across all genes. Dietary Se affected (P < 0.05) 2, 3, 3, 5, 6, 7, 7, and 8 selenoprotein genes in muscle, hypothalamus, liver, kidney, heart, spleen, thyroid, and pituitary, respectively. Protein abundance of Gpx1, Sepp1, Selh, and Sels in 6 tissues was regulated (P < 0.05) by dietary Se concentrations in 3 ways. Compared with those fed 0.3 mg Se/kg, pigs fed 3.0 mg Se/kg became hyperinsulinemic (P < 0.05) and had lower (P < 0.05) tissue levels of serine/threonine protein kinase. In conclusion, dietary Se exerted no global regulation of gene transcripts or protein levels of individual selenoproteins across porcine tissues. Pigs may be a good model for studying mechanisms related to the potential prodiabetic risk of high-Se intake in humans.

High Dietary Selenium Intake Alters Lipid Metabolism and Protein Synthesis in Liver and Muscle of Pigs

“…Alterations of these factors were associated with expressions of 12 selenoproteins (1,3,5,9,18,19). However, to the best of our knowledge, there was no information on effects of dietary selenium, in particular high selenium intake, on body protein metabolism, although protein synthesis was reported to negatively regulate insulin sensitivity (20,21) and a high protein diet inhibited the development of type 2 diabetes (22).…”

“…At the end of Expt. 2, all pigs were killed after overnight (8 h) food deprivation (5) to collect samples of liver, muscle (longissimus dorsi), and adipose tissue (retroperitoneal fat) (5). The samples were snap-frozen in liquid nitrogen and stored at 280°C until analyses.…”

“…Although dietary selenium restriction in mice ameliorated most of the phenotypes (2), prolonged feeding of a high-selenium diet (3 mg Se/kg) caused mild gestational diabetes in pregnant rats and insulin resistance in their offspring (3). Likewise, 2 pig studies (4,5) showed the potential of high selenium intakes in causing hyperinsulinemia. Furthermore, several large human studies showed an alarming association between a high selenium intake and/or body selenium status and increased risk of hyperglycemia, hyperlipidemia, or type 2 diabetes (6)(7)(8).…”

“…Pigs represent an excellent model to study human nutrition and medicine because of their great similarities in digestive systems (33), nutrient metabolism, and responses to high selenium intakes (4,5). Furthermore, pigs are an important food-producing species worldwide, and selenium supplementation is required in diets for pigs.…”

Selenium and diabetes - evidence from animal studies

“…First, many of the past animal studies used diabetic animals [29][30][31][32][33][34][35][36][37][38][39], but the present studies have been conducted in normal animals [53,[57][58][59][60][62][63]. Second, the past experiments used high or nearly toxic doses of Se (0.9-4.5 mg/kg body weight) [29][30][31][32][33][34][35][36][37][38][39], while recent experiments used Se levels not exceeding their maximal tolerable limits (≤33.0 mg Se/kg diet).…”