Published online May 15, 2021. doi: 10.4239/wjd.v12.i5.658
Peer-review started: February 2, 2021
First decision: February 27, 2021
Revised: March 10, 2021
Accepted: April 21, 2021
Article in press: April 21, 2021
Published online: May 15, 2021
Processing time: 92 Days and 14.4 Hours
The diabetic damage of enteric neurons and intestinal capillaries supplying the enteric ganglia are strictly intestinal region dependent. Therefore, the underlying molecular differences in the neuronal environment should be more emphasized.
To prove the presence of essential regional differences in the neuronal milieu which may explain the gut segment-specific enteric neuropathy and vascular dysfunction.
To reveal the impact of diabetes and immediate insulin treatment on the thickness of basement membrane (BM) surrounding myenteric ganglia, as well as the expression of matrix metalloproteinase 9 (MMP9) and its tissue inhibitor of metalloproteinase 1 (TIMP1) which are key players in regulating extracellular matrix dynamics.
Electron microscopic morphometry, fluorescent and gold-labelling immunohisto
In the diabetic ileum, the ganglionic BM was significantly thickened which was prevented by insulin treatment. These changes were also reflected in a decrease in MMP9/TIMP1 ratio in ileal myenteric ganglia. However, in the duodenum of diabetics neither the ganglionic BM thickness nor the MMP9/TIMP1 ratio were changed.
Regionally decreased MMP9 expression in ganglia and region-dependent ganglionic BM thickening correlate well with intestinal segment-specific enteric neuropathy.
Based on these findings in type 1 diabetic rat model, we are planning to expand our investigations to type 2 diabetes in the future.