Diabetic gastrointestinal autonomic neuropathy: Current status and new achievements for everyday clinical practice

Dysfunction of the lower gastrointestinal tract as a complication of diabetes — a problematic issue in the diabetic care

“…In research conducted by Takuma et al it was shown that blocking RAGE receptors in mice resulted in reduced frequency of nerve complications [21]. Oxidative stress, which is greatly increased in diabetes, is currently considered an important factor in pathogenesis of gastrointestinal complications [9,22]. Disorders in hexosamine and protein kinase C (PKC) transformation pathways also play an important role in RONS production [7].…”

“…Mechanisms underlying neuropathy (autonomic and peripheral) in diabetes are highly complex, with a multifactorial etiology [6,7,9,15]. Autonomic neuropathy in diabetes is still a subject of intensive research, e.g.…”

“…It is thought that the following, among others, factors influencing pathogenesis of gastrointestinal disorders are: gastrointestinal motility disorders (due to disorders in gastrointestinal innervation), genetic factors, visceral hypersensitivity, hormonal disorders, dysregulation of the autonomic nervous system, hyperglycemia, inflammatory processes, nerve growth factors as well as autoimmune factor is also considered, particularly in etiology of gastroparesis [7][8][9]14]. Disorders in microcirculation supplying nerve fibers should also be considered an important factor [7,8,15].…”

“…Symptoms stemming from complications concerning small and large intestine are diarrhea (20%) [7][8][9] or constipation (according to various authors between 25% [7] and 60% [9] of patients), as well as other anorectal function disorders, e.g. fecal incontinence or visceral sensitivity disorders [10][11][12].…”

“…The nNOS neurons produce nitric oxide (NO), which is a non-adrenergic, non-cholinergic, primary, inhibitory neurotransmitter, intermediating in relaxation of gastrointestinal smooth muscles and therefore playing an important role in motility [8,13]. There is most likely an inhibition of nNOS expression by advanced glycation end products (AGEs) binding to nerve plexuses [9].…”