O diabetes como modelo de envelhecimento precoce em gliócitos corticais em camundongos

Abstract

Diabetes mellitus is a chronic disease that occurs when the pancreas does not produce enough insulin (type 1) or when insulin produced cannot be adequately used by the body, characterizing insulin resistance (type 2). Evidence shows that both brains of older animals and younger animals with diabetes present changes in the level of gene expression associated with changes in chromatin structure. The aim of the present study was to analyze and compare the patterns of chromatin organization in cortical gliocytes of young and adult diabetic mice as well as in young, adult and pre-elderly non-diabetic mice. To this end, images captured from nuclei of gliocytes isolated from female Balb/c mice and both normoglycemic and hyperglycemic female NOD mice of different ages were analyzed using ImageJ, to obtain geometric, absorbance and textural parameters. Hyperglycemic mice presented more decondensed nuclei than normoglycemic mice. Previously compact of chromatin were decompacted, suggesting that hyperglycemia induced reorganization and redistribution of chromatin in glycocytes. In addition, the nuclei of hyperglycemic animals showed a deviation from the perfect round form. Like hyperglycemia, aging was also characterized by chromatin decondensation and deviation from the perfect round form of nuclei. Aging also affected Feulgen values (estimate of DNA) in both normoglycemic and hyperglycemic animals The results of this study show that both aging and hyperglycemia cause chromatin changes and these changes are similar.