Protective effect of vitamin E against alloxan-induced mouse hyperglycemia

Biochim Biophys Acta. 2016 Apr;1862(4):647-650. doi: 10.1016/j.bbadis.2015.12.022. Epub 2015 Dec 23.

Abstract

Background: Alloxan induces oxidative stress and hyperglycemia in animal models. Acatalasemic (catalase deficiency) mice are susceptible to alloxan-induced hyperglycemia. As the incidence of hyperglycemia induced by alloxan was reportedly improved when mice were fed a vitamin E supplemented diet, this protective effect was examined.

Methods: Acatalasemic and normal mice fed a vitamin E supplemented diet were treated with alloxan. The pancreas were examined with microscopy. We also isolated pancreatic islets of normal mice treated with alloxan. The glucose stimulated insulin secretion was examined.

Results: Vitamin E powerfully ameliorated the increase in apoptosis. Vitamin E increases insulin amounts secreted from pancreatic cells, but does not ameliorate the regulation of the glucose stimulated insulin secretion.

Conclusions: It is suggested that the difference in the mice fed vitamin E supplemented diet is due to an increase of insulin secretion and that vitamin E supplementation may have a role in helping to slow the stages of diabetes mellitus.

Keywords: Alloxan; Apoptosis; Beta-cell; Hyperglycemia; Insulin; α-Tocopherol.

MeSH terms

  • Acatalasia / genetics
  • Acatalasia / metabolism
  • Acatalasia / pathology
  • Alloxan / toxicity*
  • Animals
  • Apoptosis / drug effects*
  • Apoptosis / genetics
  • Hyperglycemia / chemically induced
  • Hyperglycemia / metabolism
  • Hyperglycemia / pathology
  • Hyperglycemia / prevention & control*
  • Insulin / genetics
  • Insulin / metabolism*
  • Male
  • Mice
  • Pancreas / metabolism*
  • Pancreas / pathology
  • Vitamin E / pharmacology*

Substances

  • Insulin
  • Vitamin E
  • Alloxan