Clinical Research
Copyright ©2007 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Sep 28, 2007; 13(36): 4881-4890
Published online Sep 28, 2007. doi: 10.3748/wjg.v13.i36.4881
Impaired contractility and remodeling of the upper gastrointestinal tract in diabetes mellitus type-1
Jens Brøndum Frøkjær, Søren Due Andersen, Niels Ejskjær, Peter Funch-Jensen, Asbjørn Mohr Drewes, Hans Gregersen
Jens Brøndum Frøkjær, Søren Due Andersen, Asbjørn Mohr Drewes, Center for Visceral Biomechanics and Pain, Aalborg Hospital, Aalborg, Denmark
Jens Brøndum Frøkjær, Department of Radiology, Aalborg Hospital, Aalborg, Denmark
Niels Ejskjær, Department of Endocrinology M, Aarhus University Hospital, Aarhus, Denmark
Peter Funch-Jensen, Department of Surgical Gastroenterology L, Aarhus University Hospital, Aarhus, Denmark
Asbjørn Mohr Drewes, Hans Gregersen, Center for Sensory-Motor Interaction, Department of Health Science and Technology, Aalborg University, Denmark
Hans Gregersen, National Center for Ultrasound in Gastro-enterology, Haukeland University Hospital, Bergen, Norway
Author contributions: All authors contributed equally to the work.
Correspondence to: Jens Brøndum Frøkjær, MD, PhD, Center for Visceral Biomechanics and Pain, Department of Radiology, Aalborg Hospital, DK-9100 Aalborg, Denmark. jf@mech-sense.com
Telephone: +45-99326825
Received: February 20, 2007
Revised: March 12, 2007
Accepted: March 21, 2007
Published online: September 28, 2007
Abstract

AIM: To investigate that both the neuronal function of the contractile system and structural apparatus of the gastrointestinal tract are affected in patients with longstanding diabetes and auto mic neuropathy.

METHODS: The evoked esophageal and duodenal contractile activity to standardized bag distension was assessed using a specialized ultrasound-based probe. Twelve type-1 diabetic patients with autonomic neuropathy and severe gastrointestinal symptoms and 12 healthy controls were studied. The geometry and biomechanical parameters (strain, tension/stress, and stiffness) were assessed.

RESULTS: The diabetic patients had increased frequency of distension-induced contractions (6.0 ± 0.6 vs 3.3 ± 0.5, P < 0.001). This increased reactivity was correlated with the duration of the disease (P = 0.009). Impaired coordination of the contractile activity in diabetic patients was demonstrated as imbalance between the time required to evoke the first contraction at the distension site and proximal to it (1.5 ± 0.6 vs 0.5 ± 0.1, P = 0.03). The esophageal wall and especially the mucosa-submucosa layer had increased thickness in the patients (P < 0.001), and the longitudinal and radial compressive stretch was less in diabetics (P < 0.001). The esophageal and duodenal wall stiffness and circumferential deformation induced by the distensions were not affected in the patients (all P > 0.14).

CONCLUSION: The impaired contractile activity with an imbalance in the distension-induced contractions likely reflects neuronal abnormalities due to autonomic neuropathy. However, structural changes and remodeling of the gastrointestinal tract are also evident and may add to the neuronal changes. This may contribute to the pathophysiology of diabetic gut dysfunction and impact on future management of diabetic patients with gastrointestinal symptoms.

Keywords: Diabetes; Autonomic Neuropathy; Bio-mechanics; Contractility; Ultrasound; Esophagus; Duodenum; Deformation; Stress