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Dystroglycan patterns on the prostate of non‐obese diabetic mice submitted to glycaemic control
Author(s) -
Cag Quitete Valéria Helena Alves,
Fávaro Wagner José
Publication year - 2009
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/j.1365-2613.2008.00624.x
Subject(s) - endocrinology , medicine , prostate , diabetes mellitus , nod mice , insulin , stromal cell , receptor , extracellular matrix , nod , biology , microbiology and biotechnology , cancer
Summary Dystroglycan (DG) is an adhesion protein which plays a crucial role in the maintenance of tissue integrity. Diabetes has been pointed out as a disease which causes harmful effects on prostate function. Therefore, the main objective of this work was to verify DG distribution and structure features in diabetic mice with and without glycaemic control and to relate these parameters to prostate pathogenesis. Thirty mice (Nod and BALB/c) were divided into three groups after 20 days of diabetic state: the control group received a 5 ml/kg dose of physiological saline daily for 20 days; the diabetic group had the same treatment as the control group; the diabetic‐insulin group received 4–5 IU doses of Neutral Protamine Hagedorn (NPH) insulin daily for 20 days. After 20 days of treatment, all animals were killed and samples from the ventral prostate were processed for immunological and light microscopy analyses. The results showed diminished β‐ and α‐DG receptors in the diabetic group. However, there was a recovery of both β‐and α‐DG receptor immunolocalization after insulin administration. Epithelial and stromal morphological changes were verified in the diabetic group, which also presented recovery after insulin treatment. Thus, it could be concluded that diabetes disturbed prostate structure integrity and altered the occurrence of α and β‐DG receptors, indicating decreased cell‐matrix extracellular and cell‐basal membrane attachment. However, insulin treatment could partially restore glandular homeostasis. The decrease in epithelial–stromal interaction certainly predisposes this gland in diabetic mice to be a prostate disease target.