Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Basal and pentagastrin-stimulated gastric acid secretion and basal serum gastrin level were investigated in 55 active duodenal ulcer patients with antral colonization with Helicobacter pylori (HP) and 17 patients without. Our study shows that basal (BAO) and pentagastrin-stimulated gastric acid secretion (MAO and PAO) were significantly higher in HP positive than in HP negative patients with duodenal ulcer disease. There were also a tendency to increase in basal serum gastrin concentration in HP positive patients. We suggest that antral HP increases antral gastrin release and gastric secretion. Increased acid secretion then causes duodenal ulcers by producing a low intraduodenal pH.
Zhonghua Nei Ke Za Zhi 1991 Jun
PMID:[Duodenal ulcer disease: Helicobacter pylori and hyperchlorhydria]. 191 66

Endoscopic manometry of sphincter of Oddi (SO) and serum levels of gastrin, glucagon, and somatostatin were measured in patients with postcholecystectomy syndrome (n = 12), asymptomatic cholecystectomy patients (n = 6), and controlled subjects (n = 14). Pentagastrin-stimulated gastric acid secretion test was also performed in part of patients who had symptoms or no symptoms after the removal of gallbladder. The results showed that the patients of symptomatic group had hypertonic dyskinesia of SO as shown by deep and wide waves superimposed on high basal pressure plateau of SO. The symptomatic group also had a higher serum level of gastrin and a greater BAO than those of other two groups. No difference of serum levels of glucagon and somatostatin was found among these three groups. The hypertonic dyskinesia of SO and hypergastrinemia are possibly important factors in the pathogenesis of postcholecystectomy syndrome.
Zhonghua Nei Ke Za Zhi 1991 Jun
PMID:[A study on motility of sphincter of Oddi in postcholecystectomy syndrome]. 191 67

Thirty patients with bile reflux gastritis, proven by gastroscopy and Milk 99mTc-EHIDA Test, were studied and their clinical features were compared with those of patients with non-bile reflux gastritis. The symptoms were similar in both groups of patients, whereas histologically in bile reflux gastritis there were more hyperemia of mucosa, more obvious edema in lamina propria and more polymorphonuclear infiltration. Furthermore, in bile reflux gastritis the histological changes were more severe in the antrum and decreased in severity toward the cardia. Acid secretion was significantly lower in patients with bile reflux gastritis than in patients with non-bile reflux gastritis while the serum gastrin level was significantly higher in the former than in the latter group. The authors suggest that there may be a vicious cycle among duodenogastric reflux, low level of gastric acidity and high level of serum gastrin. When duodenogastric reflux occurs, not only the bile salts damage the gastric mucosa and subsequently cause the back diffusion of hydrogen ion but also the alkaline duodenal juice neutralizes the gastric acid, resulting in decrease of gastric acidity. The bile salts and low acidity can stimulate the release of serum gastrin which antagonizes the effects of cholecystokinin and secretin on pyloric tone and aggravates the duodenogastric reflux.
Zhonghua Nei Ke Za Zhi 1989 Feb
PMID:[Clinical characteristics of bile reflux gastritis]. 273 41

An animal ulcer model resembling human peptic ulcer elicited with neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by different routes of administration, i.e., intracerebroventricular (i.c.v.), subcutaneous (s.c.) or intraperitoneal (i.p.) injections was newly established. MPTP given in multiple daily doses by either i.c.v., s.c. or i.p. produced 50%-100%, 75% and 100% gastric or duodenal ulcers respectively with low mortality and was indicative of a better animal model in elucidating the correlation between neurotransmitters and ulcer diseases. This compound decreased total gastric acid output, increased the combined mucus secretion and serum gastrin, but had little effect on secretion of free gastric acid. Thus these results showed that MPTP-induced gastroduodenal ulcers are possibly associated with impaired defensive ability of mucosa, especially of mucus bicarbonate barrier instead of gastric acid. However, further study is needed to demonstrate why administration of the drug in different routes produced different ulcers.
Zhonghua Nei Ke Za Zhi 1994 May
PMID:[An animal model of peptic ulcer induced by destruction of dopaminergic neurons]. 783 42

Acute and chronic effect of Radix Angelicae Sinensis (RAS) on serum gastrin levels in patients with cirrhosis were investigated. The results showed that after intravenous perfusion of RAS, serum gastrin levels of inferior vana cava, hepatic and peripheral veins were significantly decreased. After long-term administration of the agent, the level fell nearly to that of control subjects. It is suggested that the effect of reducing serum gastrin level by RAS may improve portal hemodynamics and be beneficial for portal hypertensive gastroduodenal mucosal lesions in cirrhosis.
Zhonghua Nei Ke Za Zhi 1994 Jun
PMID:[Effect of radix Angelicae sinensis on serum gastrin levels in patients with cirrhosis]. 786 24

To define the clinical and pathological characteristics of Helicobacter pylori-associated gastritis, 173 patients with chronic gastritis, including 99 Hp-positive and 74 Hp-negative patients were studied. We found that there were no significant differences between Hp-positive and Hp-negative patients with regard to clinical symptoms, gastric acid secretion and serum basal gastrin level, whereas the grades of chronic gastritis and active gastritis were markedly higher in Hp-positive patients. 91.2% of patients with active gastritis had evidence of Hp infection. With the increase in Hp density, the proportion of high grades (II and III) gastritis tended to increase, especially the severe active gastritis. In addition, glandular atrophy and intestinal metaplasia in antral mucosa were significantly commoner in Hp-positive patients. There were no significant differences between the two groups in duodenogastric reflux rate, but the reflux rate over moderate degree in Hp-positive patients (19.59%) was somewhat lower that in Hp-negative patients (36.36%) (P = 0.09).
Zhonghua Nei Ke Za Zhi 1993 Oct
PMID:[Clinical and pathological characteristics of Helicobacter pylori-associated chronic gastritis]. 815 40