Biomechanical and morphometric intestinal remodelling during experimental diabetes in rats

Abstract

Aims/hypothesis. Morphometric and passive biomechanical properties were studied in the duodenum, jejunum and ileum in 10 non-diabetic and 40 streptozotocin-induced diabetic rats. Methods. The diabetic rats were divided into groups living 4 days, 1, 2, and 4 weeks after diabetes was induced (n=10 for each groups). The mechanical test was done as a ramp distension experiment. The intestinal diameter and length were obtained from digitised images of the intestinal segments at pre-selected pressures and at no-load and zero-stress states. Circumferential and longitudinal stresses (force per area) and strains (deformation) were computed from the length, diameter and pressure data and from the zero-stress state geometry. Results. The blood glucose concentration increased four-to fivefold in the diabetic rats. Streptozotocin-induced diabetes generated pronounced increase in the weight per centimetre length, wall thickness and wall cross-sectional area in all intestinal segments during diabetes (p<0.05). Histological analysis showed that the thickness of the intestinal layers was increased in all segments during diabetes (p<0.05). In the duodenum the opening angle did not change in the first 2 weeks and decreased after 4 weeks (p<0.05). In the jejunum and ileum the opening angle increased after 1 week in the diabetic group. The residual strain showed the same pattern as the opening angle. Furthermore, it was found that the circumferential and longitudinal stiffness of the intestinal wall increased with the duration of diabetes (p<0.05 and p<0.01). Conclusion/interpretation. Morphological and biomechanical remodelling of the small intestine occurred during the development of diabetes. [Diabetologia (2003[Diabetologia ( ) 46:1688[Diabetologia ( -1697

Biomechanical and Histomorphometric Colon Remodelling in STZ-Induced Diabetic Rats

“…Therefore, STZ-induced diabetes in rats is a relevant model to study the remodelling of the colon during the development of diabetes. Using this model, our group demonstrated that morphological and biomechanical remodelling occurs in the oesophagus [6][7][8] and small intestine [8][9][10][11]. Furthermore, the biomechanical properties in the normal rat colon were reported [12].…”

“…The experimental procedures are similar to those reported by us before [8,11]. Briefly, the rats were anaesthetized with Hypnorm 0.5 mg and Dormicum 0.25 mg per 100 g body weight (Hypnorm:Dormicum:sterile water = 1:1:2; subcutaneous injection).…”

Effects of L-glutamine supplementation on the myenteric neurons from the duodenum and cecum of diabetic rats

“…Diabetes mellitus is defined as a chronic disease characterized by metabolic disorders in which hyperglycemia and glucose intolerance are the main characteristics (22,43) . Hyperglycemia disrupts the normal metabolism of cells, inducing the formation of reactive oxygen species, and also decreases the levels of cellular glutathione, an endogenous antioxidant (34) .…”

“…Diabetic neuropathy is a heterogeneous group of disorders that causes a variety of abnormalities (37) which may affect the autonomic and peripheral nervous system harming quality of life (1,20,36) . The most common complications include dysphagia, reflux, constipation, abdominal pain, nausea, vomiting, and diarrhea (16,43) . The development and severity of diabetic neuropathy is related to the duration of diabetes and reduction of metabolic control (21) .…”

Advanced glycation end-product expression is upregulated in the gastrointestinal tract of type 2 diabetic rats

“…The pathogenesis of such symptoms in diabetes mellitus is complex, multi-factorial with motor dysfunction, glycemic control, autonomic neuropathy, and psychological factors, and is not well understood [4] . Previous studies demonstrated changes in the morphological and biomechanical properties of the GI tract during diabetes, e.g., the wall thickness and stiffness of GI tract increased [5][6][7] . The structure or deformation changes may alter the relative positions of the mechanosensitive afferents (zero setting of the mechanosensitive afferents).…”