Open AccessEffects of experimental diabetes on the structure and ultrastructure of the coagulating gland of C57BL/6J and NOD mice
Author(s) -
Carvalho C.A.F.,
Camargo A.M.,
Cag V.H.A.,
Padovani C.R.
Publication year - 2003
Publication title -
the anatomical record part a: discoveries in molecular, cellular, and evolutionary biology
Language(s) - English
Resource type - Journals
eISSN - 1552-4892
pISSN - 1552-4884
DOI - 10.1002/ar.a.10014
Subject(s) - ultrastructure , nod , nod mice , diabetes mellitus , microbiology and biotechnology , chemistry , medicine , endocrinology , biology , anatomy
Abstract Diabetes mellitus can lead to reproductive disorders that in turn result in weakened fertility brought about by morphofunctional changes in the testes and accessory sex glands. However, doubts persist concerning the basic biology of the secretory epithelial cells and the stroma of the coagulating gland of diabetic mice. Thus, the objective of the present study was to analyze the histological and ultrastructural changes associated with stereology of the coagulating gland of mice with alloxan‐induced diabetes, and of spontaneously diabetic mice. Sixteen mice of the C57BL/6J strain, and eight non‐obese diabetic (NOD) mice were used. The animals were divided into three groups: 1) control (C), 2) alloxan diabetic (AD), and 3) NOD. Thirty days after the detection of diabetic status in group 2, all of the animals were killed and then perfused with Karnovsky's solution through the left cardiac ventricle. The coagulating gland was then removed and processed for morphometric study by light microscopy and electron microscopy. The results showed thickening of the stroma, atrophy of secretory epithelial cells, and disorganization of the organelles involved in the secretory process in both NOD and alloxan‐induced mice. Thus, it may be concluded that the coagulating gland suffered drastic morphological changes, and consequently impaired glandular function, in the presence of diabetes mellitus type I in both NOD and AD mice. Anat Rec Part A 270A:129–136, 2003. © 2003 Wiley‐Liss, Inc.