Published online Apr 15, 2024. doi: 10.4239/wjd.v15.i4.758
Peer-review started: December 12, 2023
First decision: January 15, 2024
Revised: January 29, 2024
Accepted: March 11, 2024
Article in press: March 11, 2024
Published online: April 15, 2024
Epidemiological studies have shown several long-term neurological, cardiovascular, and endocrinological complications of gestational diabetes mellitus (GDM) in offspring.
Although there are several reports about the metabolic long-term complications of GDM on offspring, there is scarce information about the pathological changes at a cellular level that occur in the pancreas of offspring born from dams with GDM.
To quantify a subset of sensory and sympathetic nerve fibers, macrophages, and vasculature in the pancreas from adult offspring born from mouse dams with GDM.
GDM was induced by i.p. administration of streptozotocin (STZ) in ICR mouse dams. Adult female offspring born from dams with and without GDM were sacrificed and pancreata were processed for immunohistochemistry. There was a quantification of the density of sensory (CGRP) and sympathetic (TH) axons, blood vessels (endomucin), and macro-phages (CD68) in the splenic pancreas using confocal microscopy.
Offspring mice born from STZ-treated dams had similar body weight and blood glucose values compared to offspring born from vehicle-treated dams. However, the density of CGRP+ and TH+ axons, endomucin+ blood vessels, and CD68+ macrophages in the exocrine pancreas was significantly greater in offspring from mothers with GDM vs control offspring. Likewise, the microvasculature in the islets was significantly greater, but not the number of macrophages within the islets of offspring born from dams with GDM compared to control mice.
GDM induces neuronal, vascular, and inflammatory changes in the pancreas of adult progeny, which may partially explain the higher propensity for offspring of mothers with GDM to develop metabolic diseases.
Future studies are needed to evaluate the functional implications of these alterations and determine if their blockade with mechanism-based therapies may decrease the risk of developing impaired glucose tolerance and type-2 diabetes in individuals born from women with GDM.