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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Streptozotocin-Induced Maternal Hyperglycemia Increases the Expression of Antioxidant Enzymes and Mast Cell Number in Offspring Rat Ventral Prostate

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Author(s):
Camargo, Ana C. L. ; Dos Santos, Sergio A. A. ; Rinaldi, Jaqueline C. ; Constantino, Flavia B. ; Colombelli, Ketlin T. ; Scarano, Wellerson R. ; Felisbino, Sergio L. ; Justulin, Luis A.
Total Authors: 8
Document type: Journal article
Source: Anatomical Record-Advances in Integrative Anatomy and Evolutionary Biology; v. 300, n. 2, p. 291-299, FEB 2017.
Web of Science Citations: 1
Abstract

Gestational diabetes mellitus (GDM) has increased in recent years. Although the cellular and molecular mechanisms involved in GDM-increased risk factors to offspring remained poorly understood, some studies suggested an association between an increase in oxidative stress induced by maternal hyperglycemia and complications for both mothers and newborns. Here, we investigated the impact of maternal hyperglycemia followed by maternal insulin replacement during lactation on the expression of antioxidant enzymes and mast cell number in offspring ventral prostate (VP) at puberty. Pregnant rats were divided into three groups: control (CT); streptozotocin-induced maternal hyperglycemia (MH); and MH plus maternal insulin replacement during lactation (MHI). Male offspring were euthanized at postnatal day (PND) 60 and the VP was removed and processed for histology and Western blotting analyses. Maternal hyperglycemia delayed prostate maturation, and increased mast cell number catalase (CAT), superoxide dismutase (SOD), glutatione-s-transferase (GST-pi), and cyclooxygenase-2 (Cox-2) expression in the offspring of hyperglycemic dams. Maternal insulin replacement restored VP structure, mast cell number and antioxidant protein expression, except for Cox-2, which remained higher in the MHI group. Thus, an increase in oxidative stress induced by intrauterine hyperglycemia impacts prostate development and maturation, which persists until puberty. The overall improvement of maternal metabolism after insulin administration contributes to the restoration of prostate antioxidant enzymes and secretory function. Taken together, our results highlighted that imbalanced physiological maternal-fetal interaction contributes to the impairment of reproductive performance of the offspring from diabetic mothers. Anat Rec, 300:291-299, 2017. (c) 2016 Wiley Periodicals, Inc. (AU)

FAPESP's process: 11/16522-0 - Effects of gestational diabetes on Wistar rat ventral prostate: morphometrical analysis, cellular proliferation and death and expression of androgen receptor and prostatein
Grantee:Sérgio Alexandre Alcantara dos Santos
Support type: Scholarships in Brazil - Master
FAPESP's process: 13/19673-5 - Effect of mild gestational diabetes and maternal insulin replacement on the ventral prostate of male Wistar rat offspring: oxidative stress and matrix metalloproteinases
Grantee:Ana Carolina Lima Camargo
Support type: Scholarships in Brazil - Scientific Initiation
FAPESP's process: 12/18100-9 - Effect of gestational diabetes on rat ventral prostate: morphological analysis, cellular proliferation and apoptosis and expression of androgen receptor and prostatein
Grantee:Luis Antonio Justulin Junior
Support type: Regular Research Grants