oxyntomodulin and Duodenal-Ulcer

Topics: Bicarbonates; Cholecystokinin; Duodenal Ulcer; Gastric Acid; Gastric Inhibitory Polypeptide; Gastrointestinal Hormones; Gastrointestinal Motility; Glucagon-Like Peptides; Humans; Pancreas; Pancreatic Polypeptide; Peptic Ulcer; Secretin; Somatostatin

Topics: Animals; Blood Glucose; Celiac Disease; Digestive System; Duodenal Ulcer; Gastric Inhibitory Polypeptide; Gastrointestinal Diseases; Gastrointestinal Hormones; Glucagon; Glucagon-Like Peptide 1; Glucagon-Like Peptides; Glucose Tolerance Test; Humans; Ileum; Insulin; Intestine, Small; Islets of Langerhans; Jejunum; Peptide Fragments; Peptides; Vagotomy

Progress in gut hormone research has considerably increased our knowledge in gastrointestinal physiology. However, this knowledge has not yet helped the understanding of common gastrointestinal diseases. A pathophysiological role of gut hormones has been established only for rare conditions This is because the clinical significance of the gut hormones is difficult to evaluate. Morphological and biochemical methods used in classical endocrinology can rarely be applied to gastrointestinal endocrinology because of the special design of the gut hormone system. Also gut hormones and autonomous nervous system overlap in their function. A defect of one system can be compensated by the other. Since the hormone-producing cells of the gut are stimulated by food ingestion, any functional or organic change of the digestive tract will alter gut hormone response. Accordingly, most changes of gut hormone levels are secondary. In some--apparently rare--instances such secondary changes contribute to the symptomatology of a pathological condition. In other instances gut hormone abnormalities mimic common diseases, thus demonstrating the heterogenecity of these conditions. More specific and reliable methods are needed to prove or to exclude the participation of gastrointestinal peptides in the pathogenesis of gastrointestinal disease. Gut peptides are an important link between nutrient entry and metabolism. This is realized by a hormonal gut factor (incretin) which augments glucose-induced insulin release. GIP is the most thoroughly investigated but not the only incretin. In addition, GIP seems to have direct effects on lipid metabolism. This would explain why fat releases more GIP than glucose. Except in the case of the metabolic hormones insulin and glucagon the therapeutic usefulness of gastrointestinal peptides has not yet been established.

Topics: Autonomic Nervous System; Duodenal Ulcer; Endocrine Glands; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Diseases; Gastrointestinal Hormones; Glucagon; Glucagon-Like Peptide 1; Glucagon-Like Peptides; Humans; Insulin; Insulin Secretion; Intestinal Absorption; Peptide Fragments; Peptides

Glucagon-like peptide-1 (GLP-1)(7-36) amide is an intestinal incretin hormone which also inhibits gastric acid secretion in humans. Its mechanism of action is unclear, but it strongly inhibits vagally induced secretion (sham feeding), suggesting that it could influence vagal activity.. The effect of intravenous GLP-1 (7-36 amide) (1 pmol/kg/min) was studied on pentagastrin induced acid secretion in otherwise healthy subjects, previously vagotomised for duodenal ulcer (n = 8) and in a group of young (n = 8) and old (n = 6) healthy volunteers.. Pentagastrin increased acid secretion significantly in all three groups, but the plateau concentration in the vagotomised subjects was lower than in controls. Infusion of GLP-1 (7-36 amide) significantly inhibited acid secretion in the control groups (to 67 (SEM 6) and 74 (SEM 3)% of plateau concentrations in young and old controls, respectively) but had no effect in the vagotomised subjects. Differences in plasma concentrations of GLP-1 (7-36 amide), recovery of gastric marker, duodenal regurgitation, or Helicobacter pylori status could not explain the lack of effect. Blood glucose was lowered equally by GLP-1 (7-36 amide) in all subjects.. The inhibitory effect of GLP-1 (7-36 amide) on acid secretion depends on intact vagal innervation of the stomach.

Topics: Adult; Aged; Blood Glucose; Duodenal Ulcer; Female; Gastric Acid; Gastric Mucosa; Glucagon; Glucagon-Like Peptide 1; Glucagon-Like Peptides; Humans; Male; Middle Aged; Pentagastrin; Peptide Fragments; Vagotomy

Plasma concentrations of oxyntomodulin-like immunoreactivity, a group of intestinal peptides capable of mediating an enterogastrone signal, were measured during a 24-h period in 6 duodenal ulcer patients and compared with those of 16 age-matched controls. Each subject was submitted to 18 oxyntomodulin-like immunoreactivity determinations. Four standardized meals were given during the test. Furthermore, each patient was evaluated for peak acid output after pentagastrin stimulation. The values of the duodenal ulcer subjects were predominantly within normal acid secretion limits. Fasting levels, meal-induced variations, and nocturnal production of oxyntomodulin-like immunoreactivity were similar in the two groups. A negative correlation was observed between peak acid output and oxyntomodulin-like immunoreactivity evaluated either as nocturnal production or as maximum nyctohemeral concentration. We conclude that, taken as a whole, duodenal ulcer disease is not caused by a defect in oxyntomodulin-like immunoreactivity secretion. However, this study does not rule out the possibility of a selective deficiency of these peptides in some duodenal ulcer subgroups such as hypersecretory patients.

Topics: Adult; Aged; Circadian Rhythm; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Glucagon-Like Peptides; Humans; Male; Middle Aged; Oxyntomodulin; Radioimmunoassay

Simultaneous 50-g oral glucose tolerance tests and measurements of gastric emptying time were performed in 11 duodenal ulcer patients. Gastric emptying time, measured by the gamma-camera technique, and the response of gastric inhibitory polypeptide (GIP) and enteroglucagon to the oral load showed a significant negative correlation. The GIP response and the insulinogenic index were significantly positively correlated. It is concluded that the increased GIP and insulin response to glucose among duodenal ulcer patients may be explained by increased gastric emptying, known to occur in these patients. The study has not given new information on the possible physiological role of enteroglucagon.

Topics: Adult; Aged; Blood Glucose; Duodenal Ulcer; Female; Gastric Emptying; Gastric Inhibitory Polypeptide; Gastrointestinal Hormones; Glucagon-Like Peptides; Glucose Tolerance Test; Humans; Insulin; Male; Middle Aged

Topics: Adult; Antigens; Duodenal Ulcer; Gastric Juice; Gastrointestinal Hormones; Glucagon-Like Peptides; Hormones; Humans; Pentagastrin; Stimulation, Chemical