Diabetic state affects the innervation of gut in an animal model of human type 1 diabetes

Gastrointestinal symptoms in diabetic patients are commonplace, and are bel ieved to be due, at least partly, to neuropathy of the gut. In the present study, therefore, some important neurotransmitters in the myenteric plexus were investigated in non-obese diabetic mice, an animal model of human type 1 diabetes. For this purpose, immunocytochemistry was applied on sections from antrum, duodenum and colon, subsequently quantified by computerized im age analysis. Whereas the number of vasoactive intestinal peptide (VIP)-pos itive neurons was increased in antral myenteric ganglia of diabetic mice, t here was a decreased density of nerve fibres in muscularis propria. No diff erence was seen in the VIP of duodenum and colon. Acetylcholine-containing nerve fibres showed an increased volume density in muscularis propria of an trum and duodenum, but a decreased density in colon of diabetic mice, as co mpared with controls. There was a decreased number of neurons containing ni tric oxide synthase (NOS) in myenteric ganglia of antrum and duodenum. No d ifference was seen in density of NOS-containing nerve fibres in muscularis propria. There was no difference regarding neuropeptide Y (NPY) and galanin between diabetic and control mice; nor was there any difference between pr e-diabetic NOD mice and controls regarding all bioactive substances investi gated. It is concluded that the diabetic state affects the innervation of g ut in this animal model. The present findings may be of some relevance to t he gastrointestinal symptoms seen in patients with diabetes.