ABSTRACT
Alone or in Combination with SOD1 .................................226 11.5 Sepp1 and Diabetes .......................................................................................228
11.5.1 Functions of Sepp1............................................................................228 11.5.2 Sepp1 as a Negative Regulator of Insulin Signaling ........................ 229 11.5.3 Elevation of Circulating Sepp1 Levels in T2DM Patients ................230
11.6 Other Selenoproteins, Glucose Metabolism, and Diabetes .......................... 231
Selenium (Se) is an essential nutrient for both humans and animals. This trace element has received attention for a plethora of (assumed) beneficial effects on health as well as for its unique biochemistry. Compared with other micronutrients, Se has a rather narrow “safe window” and a U-shaped dose-response curve (FairweatherTait et al., 2011; Rayman, 2012). Although European and US health authorities recommend daily intakes of around 55 μg Se (Fairweather-Tait et al., 2011) and suggest 300-450 μg Se/day as the “tolerable upper intake level” (Division for Nutrition, 2006), excessive Se intake, even below the toxic level, might still trigger adverse effects. The main chemical forms of Se are selenomethionine (SeMet) in plant foods with selenocysteine (Sec) additionally coming from meats (Rayman et al., 2008). Nutritional supplements of Se for humans and animals include SeMet, sodium selenite, sodium selenate, and Se-enriched yeast (Rayman, 2012). Metabolism of various forms of Se converges at hydrogen selenide (Rayman et al., 2008) that supplies Se for the cellular biosynthesis of selenoproteins. Expression of selenoprotein genes in tissues is highly regulated by the body Se status (Sunde and Raines, 2011).
