Selenium and diabetes--evidence from animal studies

Area of Science:

• Nutritional Biochemistry
• Metabolic Endocrinology
• Toxicology

Background:

• Previous research suggested selenium (Se) acts as an insulin mimic with antidiabetic properties.
• Recent studies indicate a paradoxical role of high selenium intake, potentially exacerbating insulin resistance and type 2 diabetes.

Purpose of the Study:

• To investigate the diabetogenic effects of elevated dietary selenium intake.
• To elucidate the mechanisms by which high selenium levels may lead to insulin resistance and diabetes-like conditions.

Main Methods:

• Animal models (mice, rats, pigs) and human trials were used to assess the impact of elevated dietary selenium.
• Analysis of selenoprotein expression and activity, intracellular reactive oxygen species (ROS) levels, and key metabolic regulators.

Main Results:

• Elevated dietary selenium intake (0.4–3.0 mg/kg) induced insulin resistance and diabetes-like phenotypes in animal models.
• High selenium increased selenoprotein activity (e.g., GPx1, MsrB1, SelS, SelP), diminishing intracellular ROS.
• This redox shift dysregulated beta-cell function, insulin secretion, and suppressed insulin signaling pathways.

Conclusions:

• Prolonged high selenium intake poses an unexpected risk for developing insulin resistance and type 2 diabetes.
• The diabetogenic mechanism involves altered selenoprotein activity, intracellular redox balance, and dysregulation of insulin signaling and metabolic pathways.
• Further research is needed to explore specific selenium metabolites, non-redox mechanisms, and the interplay between selenium, carcinogenesis, and diabetogenesis.