Deficiency of KIT‐positive cells in the colon of patients with diabetes mellitus

Abstract

Deficiency of ICC might be related to the pathogenesis of diabetic gastroenteropathy in humans.

Comparison of Changes in the Interstitial Cells of Cajal and Neuronal Nitric Oxide Synthase-positive Neuronal Cells With Aging Between the Ascending and Descending Colon of F344 Rats

“…Since mast cells are known to express KIT, they were excluded from the counts after being identified by their round or oval shape and deficiency of processes. 7,10,40 For immunostaining, an automatic immunostainer (BenchMark XT; Ventana Medical Systems, Inc, Tucson, AZ, USA) and UltraView Universial DAB detection kit (Ventana Medical Systems) were used. Sections not treated with primary antibodies were used as negative controls.…”

Advances in Research on Pacemaking Function of Interstitial Cell of Cajal in Gastrointestinal Tract

“…ICCs are associated with vagal afferent nerves (Fox et al, 2000) and hence studies into the pathophysiology of ICC associated with gastroparesis may www.intechopen.com hold the key to advancing our understanding of the causes of gut motility disorders associated with diabetes. In some patients with severe diabetic gastroparesis, the number of ICC has been shown to be significantly reduced in different parts of gut using immunohistochemistry (He et al, 2001;Nakahara et al, 2002;Forster et al, 2005;Miller et al, 2008). Damage to ICC, pacemakers, and mediators of neuromuscular neurotransmission in the gastrointestinal tract contributes to the pathogenesis of diabetic gastroenteropathy in both patients and animal models.…”

Regional Distribution of Interstitial Cells of Cajal (ICC) in Human Stomach

“…In general, ICC-MY is believed to form two dimensional networks in the neural plexuses and play a role as a pacemaker [7], whereas ICC-IM which is known to occupy only 5% of the tunica muscularis [12] is known to form synaptic connection with nerve terminals of enteric motor neurons of the stomach and play a central role, receptor inputs from motor neurons, although there are still controversies [13][14][15]. In accordance with this notion, significant reduction of density and constructional destruction of ICC with abnormal functions have been suggested to be responsible for many GI motility disorders and diseases such as constipation, infantile hypertrophic pyloric stenosis and acquired megacolon [16,17]. Indeed, ICC is widely accepted today as an essential target to be considered seriously in many of abnormal GI motility diseases.…”