Maternal hyperglycemia affects cell proliferation signalling and stromal organization in the prostate of neonatal and juvenile rat offspring.

Autor: Peixoto LFF; Department of Cell Biology, Histology and Embriology, Institute of Biomedical Sciences - ICBIM, Universidade Federal de Uberlândia, Uberlândia, Minas Gerais, Brazil., Sudário LED; Department of Cell Biology, Histology and Embriology, Institute of Biomedical Sciences - ICBIM, Universidade Federal de Uberlândia, Uberlândia, Minas Gerais, Brazil., Silva MDGCE; Department of Cell Biology, Histology and Embriology, Institute of Biomedical Sciences - ICBIM, Universidade Federal de Uberlândia, Uberlândia, Minas Gerais, Brazil., Mascarenhas FNADP; Department of Anatomy, Institute of Biomedical Sciences - ICBIM, Universidade Federal de Uberlândia, Minas Gerais, Brazil., Muniz EH; Department of Cell Biology, Histology and Embriology, Institute of Biomedical Sciences - ICBIM, Universidade Federal de Uberlândia, Uberlândia, Minas Gerais, Brazil., Zanon RG; Department of Anatomy, Institute of Biomedical Sciences - ICBIM, Universidade Federal de Uberlândia, Minas Gerais, Brazil., Ribeiro DL; Department of Cell Biology, Histology and Embriology, Institute of Biomedical Sciences - ICBIM, Universidade Federal de Uberlândia, Uberlândia, Minas Gerais, Brazil. Electronic address: daniele.ribeiro@ufu.br.
Jazyk: angličtina
Zdroj: Acta histochemica [Acta Histochem] 2024 Dec; Vol. 126 (8), pp. 152193. Date of Electronic Publication: 2024 Sep 07.
DOI: 10.1016/j.acthis.2024.152193
Abstrakt: Gestational diabetes mellitus is a common medical complication during pregnancy. It creates a hyperglycemic environment and impacts offspring development, increasing the risk of long-term complications, including obesity, impaired glucose metabolism and cardiovascular disease. The impact of gestational diabetes on the prostates of adult offspring has already been described; however, it is not known whether these effects are due only to the maternal condition or whether the offspring develop them throughout life. This investigation evaluated the prostates of neonatal and juvenile offspring of hyperglycemic rats due to diabetes. Diabetes was induced with streptozotocin (50 mg/kg, ip) in pregnant Wistar rats and the prostates of 7- or 30-day-old pups from healthy (PC7, PC30) or diabetic (PD7, PD30) mothers were evaluated. We found reduced body weight in pups of PD7 and PD30 and prostate weight in PD30. Prostate branching was not affected, but a reduction in apoptotic levels was associated with impaired acinar bud canalization in neonates. Additionally, PD7 presented reduced ERK1/2 phosphorylation, cell proliferation and collagen, but fibroblasts were increased. In PD30, there was a reduction in the area of the secretory epithelium and stroma, but the luminal area was increased. Moreover, fibroblasts, smooth muscle cells, collagen and metalloproteinase 2 were decreased in these juvenile pups. These data indicate that maternal hyperglycemia inactivates an important cell proliferation signaling pathway in the prostate in the first postnatal days (which is restored in the juvenile period), but it was not sufficient to avoid epithelial and stromal atrophy. This effect on postnatal gland development may impact the reproductive capacity of the prostate in adult life.
Competing Interests: Declaration of Competing Interest The authors declare that there is no conflict of interest that could be understood as harmful to the impartiality of the research described in this article.
(Copyright © 2024 Elsevier GmbH. All rights reserved.)
Databáze: MEDLINE
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