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Plasma Gastrin Levels (plasma + gastrin_level)
Selected AbstractsRole of melatonin in mucosal gastroprotection against aspirin-induced gastric lesions in humansJOURNAL OF PINEAL RESEARCH, Issue 4 2010P. C. Konturek Abstract:, Melatonin and its precursor, l -tryptophan, have been shown to exert gastroprotective effects in animals, but their influence on the gastric damage by aspirin (ASA) in humans has been sparingly investigated. In this study, we designed to determine the effects of melatonin and l -tryptophan on ASA-induced gastric mucosal damage, gastric microbleeding, mucosal generation of prostaglandin E2, and plasma melatonin, and gastrin levels. Three groups of healthy male volunteers (n = 30) with intact gastric mucosa received daily for 11 days either ASA alone or that combined with melatonin or tryptophan. Gastric blood loss and mucosal damage were evaluated at 3rd, 7th, and 11th days of ASA administration by endoscopy using Lanza score. ASA alone caused a marked rise of gastric damage and gastric blood loss, mainly at day 3rd and 7th, but they were significantly reduced at 11th day. Pretreatment with melatonin or tryptophan remarkably reduced ASA-induced gastric lesions and microbleeding. Gastric mucosal generation of PGE2 was suppressed by about 90% in all subjects treated with ASA alone without or with addition of melatonin or tryptophan. Plasma melatonin was markedly increased after treatment with melatonin or tryptophan plus ASA, but it was also raised significantly after application of ASA alone. Plasma gastrin levels were raised in subjects given melatonin or tryptophan plus ASA, but not in those with ASA alone. We conclude that melatonin and its precursor tryptophan given orally significantly reduce gastric lesions induced by ASA possibly due to (a) direct gastroprotective action of exogenous melatonin or that generated from tryptophan and (b) gastrin released from the gastric mucosa by melatonin or tryptophan. [source] Gastrin suppresses the interdependent expression of p16 and anion exchanger 1 favoring growth inhibition of gastric cancer cellsINTERNATIONAL JOURNAL OF CANCER, Issue 6 2010Hua Tian Abstract Our previous studies demonstrated that expression and interaction of p16 with anion exchanger 1 (AE1) in gastric cancer cells is correlated with progression and shorter survival of the cancer. In this article, the effects of gastrin on p16 and AE1 and its implication in prevention and treatment of gastric cancer were studied by molecular biology techniques, animal experiment and clinical analysis. The results showed that expression of p16 in human gastric body carcinoma was downregulated along with the progression of the cancer, suggesting the reverse correlations between gastrin and p16 in vivo. Further experiments indicated that gastrin suppressed the expression of p16 via the p16 promoter and thereafter resulted in the degradation of AE1 in gastric cancer cells. Silencing of AE1 or p16 significantly inhibited the proliferation of the cancer cells. Using a xenograft tumor model in nude mice, we showed that experimental systemic hypergastrinemia induced by the administration of omeprazole led to decreased expression of AE1 and p16 as well as to a marked growth inhibition of SGC7901 tumors. It is concluded that a moderate plasma gastrin level is beneficial to the growth inhibition of gastric cancer by suppressing the expression of AE1 and p16. This finding may have an important implication for the prevention and treatment of cancers arise in the gastric antrum. [source] Determinants of basal plasma gastrin levels in the general populationJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 11 2000Hedley G Peach Abstract Background: There is considerable variation in basal plasma gastrin levels in healthy subjects. Although high plasma gastrin levels may be causally associated with duodenal ulcer and colorectal cancer, there has been little research to identify the factors that determine basal gastrin levels in the general population. Methods:Helicobacter pylori IgG antibodies and fasting basal gastrin concentrations were measured in 134 males and 137 females who had participated in a cardiovascular disease risk factor prevalence survey and for whom frozen plasma was available. Stepwise multiple linear regression analysis was used to identify the determinants of basal plasma gastrin concentration. Results: The determinants of basal plasma gastrin concentration were H. pylori infection (B = 0.12 ± 0.03; P = 0.0001), age in deciles (B = 0.02 ± 0.01; P = 0.03), hazardous drinking (B = 0.10 ± 0.05; P = 0.07) and gender (B = 0.05 ± 0.03; P = 0.06), but not education, neighborhood socioeconomic index, smoking, body mass index, vigorous exercise or medication known to affect basal plasma gastrin concentration. Ten percent (± 3) of seropositive subjects had a high basal plasma gastrin concentration > 90 pg/mL compared with only 2% (± 1) of seronegative subjects. Conclusions:Helicobacter pylori infection is one of the few modifiable determinants of basal plasma gastrin levels in the general population. [source] | ||||||||||