Failure of the nitric oxide synthase inhibitor to stimulate duodenal bicarbonate secretion in streptozotocin-diabetic rats

Takehara, Kenji; Tashima, Kimihito; Kato, Shinichi; Takeuchi, Koji

doi:10.1016/s0024-3205(97)00102-1

Cited by 5 publications

(4 citation statements)

References 19 publications

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“…Vagal nerve dysfunction as evidence by a reduced response to sham feeding‐induced serum pancreatic polypeptide and ghrelin is seen in patients with diabetic gastroparesis 63 . Vagally mediated duodenal bicarbonate secretion was impaired at 6 weeks of diabetes in STZ‐diabetic rats 64 . The major viscerosensory information provided by afferent fibres is processed in the nucleus of tractus solitarius of the brain stem.…”

Section: Mechanisms Underlying Diabetic Enteric Neuropathymentioning

confidence: 99%

“…63 Vagally mediated duodenal bicarbonate secretion was impaired at 6 weeks of diabetes in STZ-diabetic rats. 64 The major viscerosensory information provided by afferent fibres is processed in the nucleus of tractus solitarius of the brain stem. The afferent and efferent innervation of the GI tract is adversely affected in diabetes.…”

Section: Brain Gut Interactions In Diabetesmentioning

confidence: 99%

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Diabetes and the enteric nervous system

Chandrasekharan

Srinivasan

2007

Neurogastroenterology Motil

191

158

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Diabetes is associated with several changes in gastrointestinal (GI) motility and associated symptoms such as nausea, bloating, abdominal pain, diarrhoea and constipation. The pathogenesis of altered GI functions in diabetes is multifactorial and the role of the enteric nervous system (ENS) in this respect has gained significant importance. In this review, we summarize the research carried out on diabetes-related changes in the ENS. Changes in the inhibitory and excitatory enteric neurons are described highlighting the role of loss of inhibitory neurons in early diabetic enteric neuropathy. The functional consequences of these neuronal changes result in altered gastric emptying, diarrhoea or constipation. Diabetes can also affect GI motility through changes in intestinal smooth muscle or alterations in extrinsic neuronal control. Hyperglycaemia and oxidative stress play an important role in the pathophysiology of these ENS changes. Antioxidants to prevent or treat diabetic GI motility problems have therapeutic potential. Recent research on the nerve-immune interactions demonstrates inflammation-associated neurodegeneration which can lead to motility related problems in diabetes.

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Section: Mechanisms Underlying Diabetic Enteric Neuropathymentioning

confidence: 99%

Section: Brain Gut Interactions In Diabetesmentioning

confidence: 99%

Diabetes and the enteric nervous system

Chandrasekharan

Srinivasan

2007

Neurogastroenterology Motil

191

158

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“…Normal rats receiving saline showed stable blood glucose levels during the test period. Subsequent treatment of STZ-CRS group with either Lcarnitine 500 mg/kg or vitamin E (60 mg/kg body weight) produced insignificant changes in blood glucose level, compared to SZT-induced diabetic rats, Table (1).…”

Section: Blood Glucose Levels In Stz-diabetic Ratsmentioning

confidence: 98%

Protective Role of L-Carnitine and Tocopherol Against Cold Restraint Stress Induced Gastric Lesions In Streptozotocin–Diabetic Rats

Elsayed

El-Sekelly

2007

BESPS

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In the present study, the influence of cold restraint stress (CRS)-induced gastric damage in diabetic rats, in relation to the antioxidative system was investigated. Male albino rats were used in the study, they were divided into 5 groups: i): non stressed group, ii): control CRS group, iii) diabetic CRS group (the rats of this group were injected with streptozotocin (STZ) 70 mg/kg i.p. and used 4 weeks after induction of diabetes with blood glucose levels of >350 mg/dl), iv): STZ L-carnitine pretreatment group (STZ-induced diabetic rat of this group were given L-carnitine 500 mg/kg 30 min before CRS) and v): STZ-vitamine E pretreatment group (STZ-induced diabetic rat of this group were given vitamin E 60 mg/kg body wt three weeks before CRS). The last four groups were exposed to CRS, at the end of each experiment, gastric damage was observed macroscopically. CRS induced gastric lesion, that was markedly exacerbated in STZ diabetic rats, but this aggravation was significantly suppressed by pretreatment with either L-carnitine or tocopherol (vitamin E) pretreatments. Diabetic rat stomachs showed significantly less glutathione peroxidase (GPX) activity as well as reduced glutathione (GSH) content than normal rat stomachs. In addition, the deleterious influence of diabetes on the gastric ulcerogenic response to CRS was significantly mitigated by decreasing lipid peroxidation by pretreatment with either L-carnitine or vitamin E. These results suggest that the gastric mucosa of diabetic rats is more vulnerable to cold restraint-induced injury, and the mechanism may be partly accounted for by impairment of the antioxidative system associated with a reduced GPX activity and GSH content. Based on these data, the beneficial effects of L-carnitine and vitamin E on CRS-induced mucosal injury especially in diabetics may be attributed to their antioxidative effects.

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“…The abnormal postprandial duodenal chyme transport is characterized by disturbed chyme clearance (229). Duodenal bicarbonate secretion is reduced in diabetic rats due to vagal-dependent neuronal dysfunction, and to decreased sensitivity of the bicarbonate secreting cell (230). Acute hyperglycemia inhibits gastric and pancreatic secretion, gallbladder motility and gastric emptying.…”

Section: Diabetes Mellitusmentioning

confidence: 99%

Small Bowel Review: Part II

Thomson

Jarocka-Cyrta²,

Faria³

et al. 2001

Canadian Journal of Gastroenterology

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In the past year, there have been many advances in the area of small bowel physiology and pathology. In preparation for this review, over 1500 papers were assessed. Some have been selected and reviewed, with a particular focus on presenting clinically useful information for the practising gastroenterologist. Relevant review articles have been highlighted, and important clinical learning points have been stressed. The topics are varied in scope and wherever possible show a logical progression from basic physiology to pathophysiology to clinical disorders and management.

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Failure of the nitric oxide synthase inhibitor to stimulate duodenal bicarbonate secretion in streptozotocin-diabetic rats

Cited by 5 publications

References 19 publications

Diabetes and the enteric nervous system

Diabetes and the enteric nervous system

Protective Role of L-Carnitine and Tocopherol Against Cold Restraint Stress Induced Gastric Lesions In Streptozotocin–Diabetic Rats

Small Bowel Review: Part II

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