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PubMedDate not supplied

[Advances in gastrointestinal hormones: cholecystokinin].

Cholecystokinin (CCK) and gastrin are members of an important family of gastroenteropancreatic polypeptides. Distribution of CCK both in the digestive system and central and peripheral nervous structures correlates with the variety of its actions; more than a classic hormone, CCK is a peptidergic neurotransmitter. CCK plays a predominant role in multiple digestive functions: contraction and emptying of the gallbladder, stimulation of pancreatic secretion of enzymes, delay of gastric emptying, diminution of gastric acid secretion, regulation of insulin secretion, reduction of food intake, etc. Distinction between pharmacologic and physiologic effects has been difficult in all of these areas. Modern technological procedures have generated significant progresses: reliable plasmatic bioassay, understanding of molecular heterogeneity, identification and characterization of receptors and their subtypes, agonists and antagonists, some of them currently available for research studies. The integrationist perspective of normal and pathological physiology has been considerably enhanced. Therapeutic use of CCK and its derivatives in some specific problems, i.e. obesity and anorexia, remains incipient and restricted.

Cholecystokinin↗
PubMed1977

[Gastrointestinal hormones. I. Hormones of the gastrin group].

Gastrin is a peptide hormone originating from G-cells of the antrum, the duodenum and the proximal jejunum. From extracts of gastrinomas and from sera of hypergastrinaemic subjects several gastrin molecules could be isolated which were nominated as "mini gastrin" (G13), "little gastrin" (G17), "big gastrin" (G34) and "big big gastrin". Antisera used for radioimmunological gastrin determinations should be characterized with respect to their specificity, as differeing affinity towards the various gastrins and towards CCK-PZ influences the results of the assay and thus the comparability with values of other laboratories. Gastrin is released by direct vagal stimulation of the antral G-cells and by local chemical and physical stimuli in the antrum and duodenum; probably an oxynto-pyloric reflex also exists. Gastrin stimulates in physiologic doses gastric acid secretion and, as shown in dogs and cats, reveals a trophic action on parietal cell growth. H+-secretion and gastrin release are connected by a feed back mechanism, insofar, as a decrease of intragastric pH below 3 inhibits endogenous gastrin release. Hypergastrinaemia has been demonstrated in patients with gastric anacidity or hypo-secretion, benigne pyloric stenosis, uraemia, short bowel-syndrome, gastric and duodenal ulceration and in patients with gastrinomas (Zollinger-Ellison-syndrome). Hypergastrinaemia in combination with hypersecretion exhibits clinical significance in patients suffering from Zollinger-Ellison-syndrome or excluded antrum syndrome which are due to autonomous gastrin release. The differential diagnosis between these syndromes and other diseases, in which hypergastrinaemia is not associated with gastric hypersecretion, can be achieved by several tests using calcium infusion or intravenous application of secretin and glucagon. The significance of elevated gastrin levels in patients with duodenal ulceration (DU) is pointed out. In DU-patients basal and postprandial hypergastrinaemia has been observed. In these patients gastrin release from gastric and extragastric sites is increased. In these patients hypergastrinaemia due to extragastric gastrin release could cause gastric hypersecretion at a time, when the stomach already has emptied. Furthermore parietal cell hyperplasia could be the result of chronic hypergastrinaemia.

Antibody Formation↗
PubMed1998

[Hormonally active peptides].

The article reviews hormonally active peptides, mechanisms of their biosynthesis and chemical synthesis. Special attention is given to achievements of the Czech school of peptidology. Mechanisms of activity of peptidergic hormones is based mainly on the activation of adenylatcyclase and formation of the "second messenger", cAMP. Other three possible mechanisms are also reviewed. Main groups of peptidergic hormones (neurohypophyseal hormones, hypothalamic regulatory hormones, gastrointestinal hormones, natriuretic peptides, and many others) are described and their therapeutic and diagnostic significance is summarised. Future prospects of peptidology in the clinical praxis are briefly reviewed.

Gastrointestinal Hormones↗
PubMed1986

Dietary protein effects on cholesterol and lipoprotein concentrations: a review.

Different dietary proteins exert different effects on plasma cholesterol concentrations. Animal studies have shown that animal proteins, most notably casein, increase plasma total cholesterol concentrations compared with vegetable proteins, such as soy. Soy protein has been shown to be hypocholesterolemic in rats, swine, primates, and rabbits. Epidemiologic studies have disclosed that vegetarians have lower mean plasma cholesterol concentrations than populations consuming diets of mixed proteins, but it is unclear whether this effect results specifically from the animal or vegetable nature of the protein. In human clinical experiments, substituting soy protein for mixed protein reduces plasma total cholesterol concentration in hypercholesterolemic subjects, but it causes only a small, nonsignificant change in persons with normal plasma cholesterol concentrations. The mechanism responsible for the effects of different proteins on plasma cholesterol concentrations has not been established. One hypothesis suggests that animal proteins, which have a greater content of phosphorylated amino acids than vegetable proteins, interfere with bile acid reabsorption. Another hypothesis suggests that the amino acid content of the protein affects cholesterol absorption, tissue storage, synthesis, and excretion. The dietary protein may also alter cholesterol metabolism by affecting plasma hormone concentrations, either postprandially or over weeks to months. Among the hormones thought to be affected by dietary protein source are insulin, glucagon, and thyroid hormones. Gastrointestinal hormones, such as gastrointestinal inhibitory polypeptide, may also be affected by dietary protein.

Amino Acids↗
PubMed1993

Effect of exogenous pancreatic enzymes on gastrointestinal and pancreatic hormone release and gastrointestinal motility.

In clinical practice, exogenous pancreatic enzymes are administered for the treatment of pancreatogenic steatorrhea or with the intention to relieve pain due to chronic pancreatitis. Moreover, a large number of patients take pancreatin (i.e., exogenous pancreatic enzymes) for functional dyspepsia. The effect of exogenous pancreatic enzymes on the enteropancreatic axis is a complex issue. Intraduodenal but not intrajejunal protease activity appears to exert a dose-dependent negative feedback on exocrine pancreatic secretion. Only enzymes with a proteolytic activity but not amylase and lipase exert a control on pancreatic secretion. The mechanism responsible for this feedback regulation is debated, but the cholinergic system seems to play a major role. Intraduodenal pancreatic enzymes (pancreatin) lead to an increased release of pancreatic polypeptide but do not affect the release of insulin and glucagon. In addition, pancreatic enzymes have an influence on the release of some gastrointestinal hormones (i.e., cholecystokinin, motilin, gastric inhibitory polypeptide). Neither exogenous nor endogenous pancreatic enzymes seem to play a major role in the regulation of interdigestive gastrointestinal motility. However, an adequate rate of postprandial pancreatic output is required to control gastric emptying. Current knowledge on the effect of exogenous pancreatic enzymes on the enteropancreatic axis, gut peptide release and gastrointestinal motility are updated in the present article.

Celiac Disease↗
PubMed1983

Effect of exorphins on gastrointestinal function, hormonal release, and appetite.

Peptic digestion of gluten results in the production of substances having opiatelike activity in bio- and receptor assays. These substances have been termed exorphins. In this study, we determined the effect of gluten, hydrolyzed gluten, and hydrolyzed gluten plus the opiate blocker naloxone on a variety of hormonal parameters, gastrointestinal transit time, small bowel mucosal integrity, and satiety. Hydrolyzed gluten prolonged intestinal transit time, and this effect was reversed by concomitant administration of naloxone. Hydrolyzed gluten also produced a naloxone-reversible increase in plasma somatostatinlike activity, which may have been responsible for the delayed transit time. No effects of the "exorphins" could be demonstrated on serum gastrin, cortisol, carbohydrate metabolism, or small bowel mucosal integrity. Although a number of studies have suggested a role for endogenous opiates in appetite regulation, we could not demonstrate any effect of "exorphins" on the amount of calories ingested nor on the perception of satiety. This study defines a potential role for small opiatelike peptides in foodstuffs in the regulation of intestinal function.

Adult↗
PubMed1998

Impact of corticotropin-releasing hormone on gastrointestinal motility and adrenocorticotropic hormone in normal controls and patients with irritable bowel syndrome.

BACKGROUND: Corticotropin-releasing hormone (CRH) plays a key role in modulating intestinal motility in stressed animals. AIMS: To evaluate the effect of CRH on intestinal motility in humans and to determine whether patients with irritable bowel syndrome (IBS) have an exaggerated response to CRH. SUBJECTS: Ten IBS patients diagnosed by Rome criteria and 10 healthy controls. METHODS: CRH (2 micrograms/kg) was intravenously administered during duodenal and colonic manometry and plasma adrenocorticotropic hormone (ACTH) was measured by radioimmunoassay. RESULTS: CRH induced motility of the descending colon in both groups (p < 0.001) and induced greater motility indexes in IBS patients than in controls (p < 0.05). CRH produced duodenal phase III motor activity in 80% of the subjects and duodenal dysmotility in 40% of IBS patients. Abdominal symptoms evoked by CRH in IBS patients lasted significantly longer than those in controls (p < 0.05). CRH induced significant increases in plasma ACTH levels in both groups (p < 0.001) and produced significantly higher plasma ACTH levels in IBS patients than in controls (p < 0.001). CONCLUSION: Human intestinal motility is probably modulated by exogenous CRH. The brain-gut in IBS patients may have an exaggerated response to CRH.

Adrenocorticotropic Hormone↗
PubMed1976

Clinical significance and perspectives of gastrointestinal peptide hormones.

Present knowledge about gastrointestinal peptide hormones is discussed from three points of view: (a) diagnostic significance of these hormones; (b) states characterized by over-production or deficiency of peptide hormones; (c) clinical application and perspectives of gastrointestinal hormones. The data in the literature are subjected to a critical analysis; in addition, the author's own experiments are discussed.

Anemia, Pernicious↗