Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The blood serum levels of gastrin and insulin and arterial blood levels of glucose were determined immediately before intravenous injection of 1 mg of glucagon, and 10, 20, 40 and 60 minutes later in 12 gastric ulcer patients, 14 duodenal ulcer patients and 12 controls using the radioimmunological and orthotoluidine methods respectively. Following glucagon administration the gastrin levels dropped in the controls and the gastrin patients, and increased in the duodenal patients by an average of 30%. Insulin levels increased in all three groups, but the increase was statistically significant in the two patients groups. Glucose levels in the blood also increased with no significant differences between the groups. It is suggested that the different effect of glucagon on gastrin levels may be due to gastrin-insulin interaction; the levels of the two hormones in the blood of duodenal patients were higher than in the other two groups studied.
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PMID:The effect of glucagon on the blood levels of gastrin, insulin and glucose in patients with gastric and duodenal ulcers. 52 17

Insulin, glucagon and C-peptide content in the blood was assayed with the use of commercial radioimmune kits (Diagnostic, USA, and Oris, France). A total of 93 peptic ulcer patients (35 with duodenal peptic ulcer, 28 with gastric ulcer, 16 after Billroth-I resection, and 14 after Billroth-II resection) and 25 patients with chronic gastritis attended by secretory insufficiency were investigated. The study was conducted on empty stomach and after a test breakfast containing 57 g of protein, 63 g of fat, 103 g of carbohydrates that comprised 1212 kcal. The highest changes in hormone incretion were recorded in patients with peptic ulcer disease after Billroth-I and Billroth-II resection, the lowest--in patients with chronic gastritis attended by secretory insufficiency.
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PMID:[Effect of food on blood levels of insulin, glucagon and C-peptide in gastroduodenal pathology]. 162 73

Low doses of insulin (less than 1.25 IU/kg body weight) stimulate gastric acid secretion in the rat, whereas higher doses (greater than 2.5 IU/kg) release gastrin and cause gastric ulcers but do not increase acid secretion. In this study we have characterized the ulcerogenic properties of insulin in the rat. A dose of 5 IU/kg subcutaneously proved to be maximally effective. Ulcer formation was rapid, and the maximum 90% incidence was reached after 5 h. Both glucose administration and food intake protected against the ulcerogenic effects of insulin. The effects of anti-ulcer drugs and of vagotomy on insulin-induced ulcers were also studied. Animals were divided into seven groups: 1) saline, 2) omeprazole, 3) ranitidine, 4) sucralfate, 5) bilateral vagotomy, 6) unilateral vagotomy, and 7) antrectomy. Medical treatment was continued for 6 days before insulin administration, operations having been performed 6-8 weeks earlier. Insulin was injected subcutaneously in a dose of 5 IU/kg. Five hours later stomachs were inspected for ulcers. Neither the antrectomized rats nor those treated with omeprazole or ranitidine had ulcers. In the saline- and the sucralfate-treated groups the gastric ulcer incidence was 83% and 80%, respectively, with a mean of six and seven ulcers per rat. Ulcers were evenly distributed between the two sides of the stomach. Rats that had undergone bilateral vagotomy (which abolishes gastric acid secretion and causes hypergastrinemia) responded to insulin with an ulcer incidence of 5%. In the unilaterally vagotomized rats there were only 2 ulcers on the denervated compared with 37 on the innervated side.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin-induced gastric ulcers in the rat. 331 Jan 98

A questionnaire was used to study the choice and use of gastric function tests by members of the British Society of Gastroenterology.Pentagastrin has largely replaced older drugs as the stimulant of choice for evoking maximal acid secretion. Insulin tests are being used in situations where they are unlikely to provide useful clinical information. Fewer physicians than surgeons measure gastric secretion, and they use tests less often. The reluctance of physicians to test patients with uninvestigated dyspepsia or gastric ulcer seems justified, but in patients having dyspepsia with negative x-ray films, or after gastrectomy or vagotomy, the greater investigative keenness of surgeons seems commendable. Only half the surgeons ever try to assess the completeness of their vagotomies, and in only one-third of this half is it their usual practice. Criticism is made of the practice of routine measurement of acid in patients with duodenal ulcer, and of the use of acid measurements to decide whether a patient should have surgery or which type of operation should be performed.
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PMID:Use of gastric function tests by British gastroenterologists. 554 Dec 30

Among an initial series of 103 patients with selective vagotomy plus pyloroplasty for duodenal ulcer, 9 patients died of causes unrelated to ulcer and 7 were lost to follow-up without signs or symptoms of ulcer 8 to 15 years after operation; the remaining 87 patients were followed up for 12 to 17 years. Insulin testing revealed only one inadequate vagotomy in a patient who had a recurrence in the short term. Insulin tests were negative in 61 and negative or adequate in 6 other patients. Complete vagotomy reduced basal secretion effectively in the great majority of patients but not in a small minority. Three patients had antral hyperfunction with persistent hypersecretion despite complete vagotomy as indicated by two negative insulin tests in each patient. Inexplicably, only one of these patients had a stomal ulcer recurrence. Long-term follow-up revealed the development of gastric ulcer in one patient wit stasis from a pyloroplasty stenosed by angulation from adhesions. Three other patients, one with ulcer and two with hemorrhagic gastritis, developed gastric ulceration in the long term despite low acid output and negative insulin tests. Biliary reflux was demonstrated in two of these three patients and was probably the cause of gastric ulcer in the third. Pre- and postoperative cholecystograms in 66 patients showed the formation of gallstones in 4 patients after vagotomy. Another patient who did not undergo cholecystography developed acute cholecystitis from stone. This rate of gallstone formation was the normal expected rate and was not increased as in some series of total vagotomy. Dumping with and without associated diarrhea was the most frequent and troublesome sequela. Postvagotomy diarrhea did not occur. To prevent dumping, and also to decrease acid secretion more effectively, pyloroplasty was abandoned in favor of Maki's pyloruspreserving antrectomy to complement selective vagotomy in 1968.
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PMID:Long-term results of selective vagotomy plus pyloroplasty. 12 to 17 year follow-up. 746 6

Gastric mucosa of diabetic rats is highly vulnerable to acute injury, but little is known about the influence of diabetic conditions on the healing of gastric ulcers. In this study, streptozotocin (70 mg/kg injected intraperitoneally) was used to induce diabetes mellitus in rats. Four weeks after streptozotocin injection, gastric ulcers were induced using the acetic acid method, and 10 days later, the healing rate and the gastric blood flow (GBF) were measured by planimetry and hydrogen (H(2))-gas clearance method, respectively. Six major groups of rats with gastric ulcers were used: (1) vehicle (saline); (2) streptozotocin alone; (3) insulin (4 IU/day intraperitoneally); (4) streptozotocin plus insulin; (5) pentoxifylline, an inhibitor of synthesis and release of tumor necrosis factor-alpha (TNF alpha); and (6) aspirin, a non-selective inhibitor of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), and rofecoxib, the highly selective COX-2. In the diabetic rats, a significant delay in ulcer healing ( approximately by 300%), accompanied by a decrease in the gastric mucosal blood flow was observed. The prolongation of the healing in diabetic animals was associated with an increase in gastric mucosal expression and release of TNFalpha, interleukin-1 beta (IL-1 beta), suppression of the vascular endothelial growth factor (VEGF), platelet endothelial cell adhesion molecule-1 (PECAM-1) and the mucosal overexpression of heat shock protein 70 (HSP 70). Administration of insulin reversed the delay in ulcer healing and significantly decreased the expression of IL-1 beta and TNF-alpha, while producing the rise in the expression of VEGF and PECAM. Pentoxifylline, an inhibitor of TNF-alpha, which by itself accelerated ulcer healing in non-diabetic rats, counteracted the increase in the area of gastric ulcer induced by streptozotocin, raised significantly gastric blood flow and suppressed the plasma TNF-alpha levels. Aspirin and rofecoxib, that significantly suppressed the mucosal prostaglandin E(2) generation in ulcer area, delayed significantly the rate of ulcer healing and decreased the GBF at ulcer margin in non-diabetic rats, and these changes were significantly augmented in diabetic animals. We conclude that: (1) Experimental diabetes dramatically impairs ulcer healing, depending upon the increased release of proinflammatory cytokines and the attenuation of angiogenesis that can limit the ulcer healing effects of locally produced HSP 70 and TNF-alpha. (2) Insulin reversed this impairment of ulcer healing in diabetic rats, mainly due to the enhancement of angiogenesis and reduction in expression of cytokines in the ulcer area. (3) Classic non-steroidal anti-inflammatory drugs such as aspirin prolonged ulcer healing under diabetic conditions due to suppression of endogenous prostaglandins and the fall in the microcirculation at the ulcer margin and these effects were mimicked by selective, so called "safe" COX-2 inhibitor, rofecoxib, suggesting that both COX isoforms are important sources of prostaglandins that are essential in the ulcer healing in diabetes.
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PMID:Impaired gastric ulcer healing in diabetic rats: role of heat shock protein, growth factors, prostaglandins and proinflammatory cytokines. 1464 93

Research in the last two decades has transformed the way hydrogen sulphide (H2S) is perceived from a noxious gas to a gaso-transmitter with a vast potential in pharmacotherapy. H2S is synthesized in various body-systems using the enzymes cystathionine beta-synthase and cystathionine gamma-lyase; either of these being the predominat enzyme in a particular system. H2S may be one of the physiological modulators of blood pressure in humans. The gas relaxes the vascular smooth muscle cells by opening up K(ATP) channels. Moreover, it suppresses the proliferation of vascular smooth muscle cells. H2S may also be contributing in the protection afforded by ischaemia-preconditioning. Testosterone is thought to be responsible for the higher central nervous system level of H2S in males. In the central nervous system, H2S is implicated in Alzheimer's disease, epilepsy, stroke and Down's syndrome. Insulin secretion is associated with a decrease in the H2S levels. Raised H2S is detrimental in acute pancreatitis as well as in septic shock. Recently, H2S-releasing derivatives of certain drugs have shown promise in protection against gastric ulcer and in inflammatory bowel disease. The beneficial effects of certain sulphur containing herbs like ginseng and garlic may be mediated via H2S. In future, development of specific drugs modulating H2S levels may prove beneficial in varied disorders.
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PMID:Gaso-transmitter hydrogen sulphide: potential new target in pharmacotherapy. 2111 45

Insulin-like growth factor 1 (IGF-1) and Akt [also known as protein kinase B (PKB)] proteins have been reported to exhibit gastroprotective effects by reducing water immersion and restraint stress (WRS)-induced gastric mucosal cellular apoptosis. To confirm whether the IGF-1/PTEN/Akt/FoxO signaling pathway is effective in protecting against gastric ulcers, our current study was conducted to examine the expression and localization of IGF-1, phosphatase and tensin homologue deleted on chromosome 10 (PTEN), Akt and O subfamily of forkhead box (FoxO) proteins, caspase-3 activity and the number of apoptotic cells in gastric mucosa of rats subjected to WRS. Our results demonstrated that WRS induced gastric ulcers by enhancing cell apoptosis in rat gastric mucosa. In addition, in normal rat gastric mucosa, PTEN, total Akt and FoxO1 were found mainly in the cell cytoplasm of fundic glands in the lamina propria close to the muscularis mucosa. In addition, strong staining of IGF-1, FoxO3a and FoxO4 in the gastric mucosa was primarily concentrated in the cell cytoplasm of the fundic glands in whole lamina propria. However, in rat gastric ulcers, IGF-1, total Akt, FoxO3a and FoxO4 were localized in proximity to the base of the ulcer margin and were also present in the granulation tissues of the gastric ulcers. Moreover, in the rat gastric ulcers, the mRNA transcript levels of IGF-1, PTEN, Akt-1, Akt-2, FoxO3 and FoxO4 were upregulated in the gastric ulcer margin, with a peak between Days 4 and 8 following 7 h of WRS. In conclusion, our results imply that the IGF-1/PTEN/Akt/FoxO signaling pathway plays a certain role(s) in the protection against ulceration through the regulation of cellular apoptosis as observed in the development and healing of rat gastric ulcers.
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PMID:Effect of the IGF-1/PTEN/Akt/FoxO signaling pathway on the development and healing of water immersion and restraint stress-induced gastric ulcers in rats. 2273 8