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. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: Free Radic Biol Med. 2013 Jul 16;65:10.1016/j.freeradbiomed.2013.07.012. doi: 10.1016/j.freeradbiomed.2013.07.012

Table 1.

Diabetogenic potential of elevated Se intakes or selenoprotein expression in animals

Treatment Finding Reference
The GPX1-overexpressing (OE) and wild type (WT) male mice (n = 80) were fed a Se-adequate diet (0.4 mg/kg) from 8 to 24 weeks of age Compared with the WT, the OE mice developed hyperglycemia, hyperinsulinemia, increased β-cell mass, hyper-secretion of insulin, insulin resistance, and obesity 22, 55
C57BL/6J mice (n = 6–7 per group) were fed either Se-deficient Torula yeast-based diet or diets supplemented with Se at 0.1 and 0.4 mg (sodium selenite)/kg of diet for 3 months Mice in the 0.4 mg Se/kg group showed decreased insulin sensitivity and hyperinsulinemia compared to those fed the Se-deficient diet and 0.1 mg of Se/kg of diet 53
Three groups of rats (n = 10) were fed either a Se-deficient diet or diets supplemented with Se at 75 or 150 μg/kg of diet for 8 weeks Rats in groups of 75 and 150 μg Se/kg diet had greater body weight, liver PTP1b activity, and liver triglyceride concentrations than the control group fed the Se-deficient diet 58
Seven groups of rats (n = 7) were fed either a Se-deficient diet or diets contained Se (as selenite or selenite) at 0.20, 1.0, and 2.0 mg/kg of diet for 8 weeks All Se-supplemented animals featured a higher body weight, elevated liver GPx1 expression and activity, increased liver PTP1b activity, and reduced PTP1b glutathionylation, compared to their Se-deficient controls 59
Female Wistar rats were fed a Se-deficient (0.01 mg/kg of diet) corn–soy basal diet (BD) or BD+Se (as Se-yeast) at 0.3 or 3.0 mg/kg of diet from 5 weeks before breeding to day 14 postpartum. Offspring (n = 8/diet) born to dams fed 0.3 and 3.0 mg of Se/kg were fed with the same respective diet until age 112 days Compared with the 0.3 mg of Se/kg of diet, the 3.0 mg of Se/kg of diet induced hyperinsulinemia, insulin resistance, and glucose intolerance in the dams at late gestation and/or day 14 postpartum and in the offspring at age 112 days 60
Weanling male pigs (n = 24) were fed a Se-deficient (< 0.02 mg of Se/kg of diet) corn-soy basal diet supplemented with 0, 0.3, or 3.0 mg of Se/kg of diet as Se-enriched yeast for 16 weeks Compared with those fed 0.3 mg of Se/kg of diet, pigs fed 3.0 mg of Se/kg of diet became hyperinsulinemic and had lower tissue levels of serine/threonine protein kinase (Akt) 62
Male pigs were fed either a Se-adequate (0.17 mg of Se/kg of diet) or a high Se (0.50 mg of Se/kg of diet) diet for 16 weeks The fasting plasma insulin and cholesterol levels were non-significantly increased in the pigs fed the high-Se diet, whereas fasting glucose concentrations did not differ between the two groups. Dietary Se oversupply affected expression and activity of proteins involved in energy metabolism in major was probably not sufficient to induce diabetes 63
Rats were intraperitoneally injected with saline (control) or 1.3, 1.6 and 3.8 mg of Se/kg of body weight as sodium selenite Sodium selenite administration caused hyperglycemia in rats and elevated plasma corticosterone levels, but did not change plasma insulin levels 57