[Effects of selenoprotein on blood glucose, Ca2+ transfer and NO system in diabetic mice]

Jun Luo1, Shi-Lian Zhang, Wei Wang

  • 1Hebei Center of Prevent and Control Disease, Shijiazhuang 050021, China.

Abstract

Insights

High-dose selenoprotein supplementation significantly reduced blood glucose and altered kidney calcium transport and nitric oxide synthase activity in diabetic mice, indicating a potential therapeutic role for selenoproteins in managing diabetes.

Area of Science:

  • Biochemistry
  • Endocrinology
  • Pharmacology

Background:

  • Diabetes mellitus is a metabolic disorder characterized by hyperglycemia.
  • Alloxan-induced diabetes in mice is a common model for studying anti-diabetic agents.
  • Selenoproteins play crucial roles in various physiological processes.

Purpose of the Study:

  • To investigate the effects of selenoprotein on blood glucose control.
  • To assess the impact of selenoprotein on calcium (Ca2+) transfer and the nitric oxide (NO) system in diabetic mice.

Main Methods:

  • A diabetic mouse model was established using alloxan injection.
  • Mice were divided into six groups, including control, diabetic, and diabetic groups treated with varying doses of selenoprotein or sodium selenite.
  • Biochemical parameters such as blood glucose, Ca2+-ATPase activity, and nitric oxide synthase (NOS) activity were measured.

Main Results:

  • The higher dose selenoprotein group (300 microg Se/kg) showed significantly lower blood glucose levels compared to the diabetic control group.
  • Kidney Ca2+-ATPase activity was significantly increased in the high-dose selenoprotein group.
  • Plasma NOS activity was significantly decreased in the high-dose selenoprotein group.

Conclusions:

  • Selenoprotein supplementation at 300 microg Se/kg effectively reduced blood glucose in diabetic mice.
  • This dose also enhanced kidney Ca2+-ATPase activity and attenuated plasma NOS activity.
  • These findings suggest selenoprotein's potential as a therapeutic agent for diabetes management.

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