Increased susceptibility of gastric mucosa to ulcerogenic stimulation in diabetic rats--role of capsaicin-sensitive sensory neurons

Author(s): Tashima K, Korolkiewicz R, Kubomi M, Takeuchi K

Abstract

1. We examined the gastric mucosal blood flow (GMBF) and ulcerogenic responses following barrier disruption induced by sodium taurocholate (TC) in diabetic rats and investigated the role of capsaicin-sensitive sensory neurons in these responses. 2. Animals were injected streptozotocin (STZ: 70 mg kg(-1), i.p.) and used after 5, 10 and 15 weeks of diabetes with blood glucose levels of > 350 mg dl(-1). The stomach was mounted on an ex-vivo chamber under urethane anaesthesia and exposed to 20 mM TC plus 50 mM HCl for 30 min in the presence of omeprazole. Gastric transmucosal potential difference (PD), GMBF, and luminal acid loss (H+ back-diffusion) were measured before and after exposure to 20 mM TC, and the mucosa was examined for lesions 90 min after TC treatment. 3. Mucosal application of TC caused PD reduction in all groups; the degree of PD reduction was similar between normal and diabetic rats, although basal PD values were lower in diabetic rats. In normal rats, TC treatment caused luminal acid loss, followed by an increase of GMBF, resulting in minimal damage in the mucosa. 4. The increased GMBF responses associated with H+ back-diffusion were mitigated in STZ-treated rats, depending on the duration of diabetes, and severe haemorrhagic lesions occurred in the stomach after 10 weeks of diabetes. 5. Intragastric application of capsaicin increased GMBF in normal rats, but such responses were mitigated in STZ diabetic rats. The amount of CGRP released in the isolated stomach in response to capsaicin was significantly lower in diabetic rats when compared to controls. 6. The deleterious influences on GMBF and mucosal ulcerogenic responses in STZ-diabetic rats were partially but significantly antagonized by daily insulin (4 units rat(-1)) treatment. 7. These results suggest that the gastric mucosa of diabetic rats is more vulnerable to acid injury following barrier disruption, and this change is insulin-sensitive and may be partly accounted for by the impairment of GMBF response associated with acid back-diffusion and mediated by capsaicin-sensitive sensory neurons.

Similar Articles

Peptic ulcer in diabetes mellitus

Author(s): Masuda H, Inoue S, Arakawa H, Koizumi K, Kubo N

Gastric mucosal damage in experimental diabetes in rats: role of endogenous glutathione

Author(s): Goldin E, Ardite E, Elizalde JI, Odriozola A, Panés J, et al.

Increased susceptibility of diabetic rat gastric mucosa to food deprivation during cold stress

Author(s): Korolkiewicz R, Tashima K, Kubomi M, Kato S, Takeuchi K

Gastric infection by Helicobacter pylori and antral gastritis in hyperglycemic obese and in diabetic subjects

Author(s): Perdichizzi G, Bottari M, Pallio S, Fera MT, Carbone M, et al.

4-Hydroxyisoleucine Experimental evidence of its insulinotropic and antidiabetic properties

Author(s): Broca C, Gross R, Petti P, Sauvaire Y, Manteghetti M, et al.

Antimutagenic and anticarcinogenic activity of Emblica officinalis

Author(s): Jose JK, Kuttan G, George J, Kuttan R

Protein measurement with the folin phenol reagent

Author(s): Lowry CH, Roosebrough NJ, Farr AL, Randall RJ

Combinatorial biosynthesis of novel antibiotics related to daptomycin

Author(s): Nguyen KT, Ritz D, Gu JQ, Alexander D, Chu M, et al.

Involvement of endogenous cholecystokinin and somatostatin in gastroprotection induced by intraduodenal fat

Author(s):  Brzozowski T, Konturek PC, Konturek SJ, Kwiecién S, Pajdo R, et al.

A new rat model of type 2 diabetes: the fat-fed, streptozotocin-treated rat

Author(s): Reed MJ, Meszaros K, Entes LJ, Claypool MD, Pinkett JG, et al.

Alpha-glucosidase inhibitory activity of Syzygium cumini (Linn

Author(s): Shinde J, Taldone T, Barletta M, Kunaparaju N, Hu B, et al.

Influence of dietary quercetin on glutathione redox status in mice

Author(s): Meyers KJ, Rudolf JL, Mitchell AE

Effect of the flavonoid quercetin on inflammation and lipid peroxidation induced by Helicobacter pylori in gastric mucosa of guinea pig

Author(s): González-Segovia R, Quintanar JL, Salinas E, Ceballos-Salazar R, Aviles-Jiménez F, et al.