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PubMed1975

The lower esophageal sphincter. Physiologic and clinical aspects.

Current concepts in physiology and pathophysiology of lower esophageal sphincteric mechanism are reviewed. With recent advances in manometric method for more accurate in-vivo human studies combined with in-vivo and in-vitro studies in animal models, there is much information regarding function of this sphincter. Three components of sphincter control have been identified: specialized circular smooth muscle at esophagogastric junction, autonomic nervous system, and probable physiology effects of gastrointestinal hormones, particularly gastrin. Clinical syndromes of sphincteric dysfunction have been identified relative to these three controlling elements. Foods and drugs that adversely effect sphincter pressure have been identified and indicate that anticholinergic agents, fatty foods, chocolate, alcohol, and cigarette smoking may have a harmful effect on a patient with heartburn. Drugs that increase the antireflux sphincter barrier have been studied. Clinical effectiveness of antacids and bethanechol in therapy of heartburn is supported by controlled treatment trials. Research continues on other medications producing increases in sphincter pressure.

Anemia, Pernicious↗
PubMed1990

Gastrointestinal peptides activate Na(+)-H+ exchanger in AR42J cells by increasing its affinity for intracellular H+.

Regulation of intracellular pH (pHi) was studied by dual wavelength fluorometry in monolayers of pancreatic AR42J cells loaded with the fluorescent probe 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. In cells superfused with N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered solution at pH 7.40, basal pHi was determined to be 7.15 +/- 0.13. Na(+)-H+ exchange could be demonstrated in both resting cells and cells subjected to acid loading by use of transient exposure to NH4Cl. Na(+)-H+ exchange was completely blocked by 300 microM amiloride and was dependent on extracellular Na+ (apparent Km = 25 mM). When the concentration of the NH4Cl pulse was varied (0.5-25 mM), the rate of pHi recovery increased as pHi became acidic, reaching a maximum of 0.007 pH units/s at pHi of 6.4. Gastrointestinal hormones, including pentagastrin, cholecystokinin, and bombesin, increased the rate of Na(+)-H+ exchange without affecting cellular buffer capacity (21.5 +/- 1.8 mM/pH unit), thereby leading to an intracellular alkalinization. This was accompanied by a shift in the curve of Na(+)-H+ exchange as a function of pHi to more alkaline values, although the maximum rate of pH recovery was unchanged. Neither protein kinase C nor Ca2+ could be conclusively linked to activation of Na(+)-H+ exchange, raising the possibility of a more direct, receptor-controlled mechanism.

Amiloride↗
PubMed1984

Secretin, VIP, and PHI stimulate rat proximal duodenal surface epithelial bicarbonate secretion in vivo.

The surface epithelial cells of the stomach and duodenum secrete bicarbonate at rest and in response to a number of agonists including the gastrointestinal hormones, glucagon, and GIP. Since those hormones with structural homology may have similar effects, the purpose of the present study was to examine the effect of graded doses (6, 24, and 96 nmol/kg) of pure porcine secretin, VIP, and PHI on bicarbonate secretion by the proximal duodenum containing Brunner's glands. Experiments were performed in vivo on unanesthetized Sprague-Dawley rats with chronic Thiry-Vella type loops of the proximal 2 cm of duodenum. The order of testing was random and only one hormone was tested on a single day. Compared to the saline control, each dose of VIP produced a significant increase in duodenal bicarbonate secretion in a dose-response manner. The two higher doses of secretin and only the 96 nmol/kg dose of PHI significantly increased bicarbonate output. The responses to 96 nmol/kg dose of secretin and VIP were similar, and each was significantly greater than observed with PHI. It is concluded that secretin and VIP stimulate proximal duodenal bicarbonate secretion and are more potent than PHI.

Animals↗
PubMed1976

Lower esophageal sphincter pressure and serum motilin levels.

The gastrointestinal hormone motilin has recently been proposed as having a physiological role in the determination of lower esophageal sphincter (LES) strength. The present study was performed to evaluate the effect of gastric alkalinization of LES pressure and serum motilin levels. Instillation of 0.1N NaHCO3 into the stomach resulted in a significant increase in LES pressure (P less than 0.01) without affecting serum motilin levels. No correlation was found between fasting serum motilin levels and resting LES pressure (r = -0.31). These observations do not support the theory that LES pressure increases during gastric alkalinization are mediated through motilin release.

Adult↗
PubMed1994

Laboratory medicine in ulcer disease.

The role of laboratory medicine in ulcer disease is poorly defined. However there is increasing evidence of the clinical usefulness of some laboratory tests that investigate secretory functions and defensive properties of the stomach, gastrointestinal hormones and Helicobacter pylori infection. These tests may modify the clinical management of patients with peptic ulcer by identifying H. pylori positive subjects, patients with high acid output, patients who do not respond to antisecretory therapy, and patients with high gastrin levels in whom Zollinger-Ellison syndrome may be suspected. Here we review the clinical value of laboratory tests in ulcer disease, particularly as concerns the cost/benefit ratio. The relative merits of these tests are described giving an indication of their possible role in the diagnostic algorithm.

Chemistry, Clinical↗
PubMed1989

Occurrence of specific receptors in the duodenum.

Three groups of receptors defined pharmacologically by means of specific agonists and competitive antagonists were described: receptors for the so-called gastrointestinal hormones, receptors for the autacoids and receptors for the neuromediators. Together with the better known post-synaptic receptors pre-synaptic ones were also discussed in the light of the different possible interactions between one and the other. The mode of action of drugs stimulating (agonists) or inhibiting (antagonists) the same receptors is so far a very intriguing problem. The availability of newer and more selective compounds capable of distinguishing not only different kinds of receptors but also the subtypes of a single class of receptors will certainly contribute to better understanding of this situation.

Duodenum↗
PubMed2001

The first PP supper--Camelot at Bispebjerg.

In the early seventies of the last century, in a temporary building called "Sukkertoppen" at Bispebjerg Hospital, a group of devoted, young medical doctors and a couple of students together with a team of highly skilled laboratory technicians gathered around the "senior" Jens F. Rehfeld, who had barely turned thirty years of age. Each person got his own peptide, raised antibodies, iodinated the peptide and established a radioimmunoassay with which he could then conquer the world of gastrointestinal hormones. It was a unique time, where old hormones had just been chemically characterized and could now be subjected to immunochemical measurements and characterization for the first time. It was also a period when a whole host of new biologically active peptides were being discovered, and basically anything you did with "your" peptide was exciting news for the scientific community. The concept of neuropeptides was being established and Jens Frederik and his brave scientific knights were in the middle of it all. The period ended in the summer of 1976, when Rehfeld moved his court to the University of Aarhus and the others scattered--each to establish their own scientific group.

Animals↗
PubMed1981

The mechanism of abnormal pancreatic beta cell response to food following acute hypoglycaemia in man.

Following acute insulin-induced hypoglycaemia, an abnormal pattern of insulin secretion in response to a meal has been demonstrated in six healthy volunteers. This is characterized by an initial impairment in insulin secretion and late hyperinsulinaemia. Postprandial gastrointestinal hormone levels were normal following hypoglycaemia in these subjects. In four other subjects, the administration of intravenous glucose prior to the meal partially reversed the abnormal pattern of secretion. In two patients with a total pre-ganglionic sympathectomy, the pattern of blood glucose, plasma insulin and C-peptide was similar to that observed following hypoglycaemia in normal subjects. It is unlikely that an abnormal entero-insular axis or an elevation of plasma catecholamine levels are primarily responsible for this phenomenon. This effect of hypoglycaemia on postprandial insulin secretion may be caused by glucopenia of the pancreatic beta cells.

Blood Glucose↗
PubMedDate not supplied

Intravenous fat emulsion (intralipid) delays gastric emptying, but does not cause gastroesophageal reflux in healthy volunteers.

The impact of overnight intravenous lipid emulsion (ILE) infusion on upper gastrointestinal tract physiology was assessed in 10 healthy volunteers. No changes in lower esophageal sphincter pressure (before infusion: 28 +/- 4 mm Hg; after infusion 20.5 +/- 3; p:NS), plasma concentrations of gastrointestinal hormones (gastrin: preprandial before/after lipids: 14 +/- 2.1/13 +/- 1.4 pM; postprandial before/after lipids: 28 +/- 2.7/30 +/- 3.4 pM, CCK: preprandial before/after lipids: 69 +/- 10/64 +/- 10 pM; postprandial before/after lipids: 96 +/- 11/95 +/- 12 pM; neurotensin: levels less than 6 pM in all samples; somatostatin levels undetectable in all samples) nor on pathologic gastroesophageal reflux episodes (% of time of pH less than 4, before/after lipids: 0.6 +/- 0.4/0.15 +/- 0.09), were found (p = NS). In contrast, technetium gastric emptying studies showed a significant delay when comparing pre- and post-lipid infusion values (37 +/- 4/54 +/- 4%) (p greater than 0.005). The mechanism of this effect remains unexplained.

Adult↗
PubMed1987

Peptide YY. Structure of the precursor and expression in exocrine pancreas.

Peptide YY is a 36-residue gastrointestinal hormone which inhibits both pancreatic and gastric secretion. We have isolated a cDNA encoding the peptide YY precursor by screening a rat intestinal lambda gt11 cDNA library with an antiserum directed against the porcine hormone. The nucleotide sequence of the cDNA encodes a 98-residue protein (molecular weight, 11, 121) which has an amino acid sequence identical to that of porcine peptide YY. Rat peptide YY is preceded immediately by a signal sequence and followed by a cleavage-amidation sequence Gly-Lys-Arg plus 31 additional amino acids. Thus the peptide YY precursor is similar in structure to that of two related peptides, pancreatic polypeptide and neuropeptide Y. RNA blot hybridizations reveal that the peptide YY gene is much more actively expressed in pancreas than previously realized. In situ hybridizations localized peptide YY cells exclusively to the exocrine pancreas. The abundance of peptide YY in one of its target organs, the pancreas, suggests a paracrine mechanism for peptide YY in regulating pancreatic enzyme secretion.

Amino Acid Sequence↗
PubMed1980

Glicentin and gastric inhibitory polypeptide immunoreactivity in endocrine cells of the gut and pancreas.

The distribution of the postulated glucagon precursor, glicentin, as well as of the gastrointestinal hormone GIP (gastric inhibitory polypeptide), has been studied by immunocytochemistry and radioimmunoassay. Our results show that GIP antisera may contain a population of antibodies recognizing an immunoreactant common to glicentin and GIP. The occurrence of such common immunoreactants makes immunological distinction between the two hormones difficult and may explain previous results indicating that GIP is stored by glucagon cells. The present results indicate that GIP is produced by endocrine cells of the duodenum and jejunem and is absent from the pancreas, stomach, and large intestine. Glicentin-like immunoreactivity is displayed by A cells of the pancreas and by oxyntic A cells of the stomach, as well as by numerous glucagon-like immunoreactant (GLI) cells of the ileum and colon. Use of glucagon ad glicentin antisera of differing specificities indicates that the processing of this putative prohormone differs between A cells and GLI cells. Studies on the ontogeny of pancreatic A cells also reveal differences in the reactivity pattern of glicentin-like immunoreactivity between fetal and adult rats. Ultraimmunocytochemical studies show that glicentin-like immunoreactivity is mainly, stored in the cytoplasmic granules of pancreatic A cells.

Aging↗
PubMed1992

Endocrine response to intragastric and intravenous glucose challenge in the denervated dog pancreas.

The functional connection between the gut and the islet cells comprises nerves and gastrointestinal hormones. In this study, we quantified the incretin effect and the glucose tolerance (KG value) before and after denervation of the pancreas in dogs in order to find out whether the incretin effect is mediated by nerves. The participation of nerves was estimated by comparing metabolic tests before and after total extrinsic pancreatic denervation in 10 dogs. Fifty-nine percent of the insulin response after intragastric glucose was calculated preoperatively to be the result of incretin factors, a value similar to the 62% found in the postoperative series (with denervated pancreas). The response of GIP to intragastric glucose was not significantly different between pre- and postoperative tests. The KG values pre- and postoperative were in the same range. From our data, we conclude that extrinsic nerves of the pancreas do not seem to play an important role in mediating glucose homeostasis in dogs.

Animals↗
PubMed2000

Nutritional implications of cephalic phase gastrointestinal responses.

Palatable cephalic stimuli induce a simultaneous activation of gastrointestinal motility, gastric acid and pancreatic enzyme secretion, as well as, release of the gastrointestinal hormones gastrin and pancreatic polypeptide. Cholinergic neural input is the dominant mediator of these responses with cholecystokinin and gastrin acting as additional stimulatory modulators. Central cholinergic circuits, neuropeptide Y, and thyrotropin releasing hormone are candidate central stimulators of the cephalic phase. There are good arguments for glucagon-like peptide-1 and peptide YY to be physiological inhibitors of cephalic-phase responses with these peptides being released in the intestinal phase of digestion and putatively contributing to termination of the cephalically stimulated pattern. Cephalic-phase responses are used clinically as diagnostic tests to assess completeness of selective proximal vagotomy and to explore autonomic neuropathy. Pancreatic polypeptide secretion with sham feeding is an appropriate test of abdominal vagal function. Cephalically stimulated motor and secretory activity contribute greater than 50% of overall postprandial responses. Pharmacological inhibition of cephalic-vagal stimulation, resulting in reduced food intake, may be a novel approach to obesity management. Glucagon-like peptide-1 is a particular candidate because it inhibits the cephalic phase of digestion, diminishes food intake, and reduces the glycemic excursion after a meal by retarding gastric emptying, stimulating insulin and lowering glucagon release.

Animals↗
PubMed1991

The effect of SMS 201-995 on meal and CCK-stimulated peptide YY release.

Somatostatin is known to inhibit the postprandial release of most gastrointestinal hormones. The aim of the present study was to evaluate the effect of an analog of somatostatin, SMS 201-995 (120 ng/kg/hr), on both meal-induced and cholecystokinin octapeptide (CCK-8, 500 ng/kg/hr)-induced peptide YY (PYY) release. Six mongrel dogs with distal ileal Thiry-Vella loops were used in this study. PYY was measured in both plasma and ileal luminal effluent. SMS 201-995 did not affect interdigestive plasma or ileal luminal PYY concentrations. CCK-8 and a fat meal both stimulated PYY release into the circulation. SMS 201-995 completely inhibited the CCK-8 and fat-stimulated circulatory release of PYY. Both CCK-8 and a mixed meal increased ileal luminal PYY recovery. SMS 201-995 inhibited CCK-8-induced, but not meal-induced, ileal luminal PYY recovery. These findings support previous studies that describe independent circulatory and ileal luminal PYY release. We conclude that both somatostatin and CCK may have a regulatory role in postprandial circulatory release of PYY.

Animals↗
PubMed1987

The role of humoral factors and the ileocecal valve in pathological changes occurring after distal small bowel resection.

Experimental studies using dogs were performed to elucidate the participation of gastrointestinal hormones as well as the ileocecal valve in postoperative sequelae following massive small bowel resection. Although in both the ileal resection and the ileocecal resection groups the absorption of fat was reduced postoperatively, body weight tended to increase in the former, while it decreased gradually in the latter. In addition, watery diarrhea persisted after ileocecal resection. Plasma total bile acid concentrations in each group were lower than those before surgery, as were plasma levels of both total glucagon and neurotensin. Although differences were not significant, plasma neurotensin levels tended to be higher after ileocecal resection, but plasma total glucagon levels tended to be lower. Plasma gastric inhibitory polypeptide (GIP) response to butter ingestion was also lower after both ileal and ileocecal resection; especially in the latter case the decrease was significant. These results indicate that the diminished plasma levels of neurotensin, enteroglucagon and GIP may be related to the impairment of adaptive changes in the remaining small intestine.

Animals↗
PubMed1984

Mechanisms of control of intestinal transport: a review.

Of the long list of substances which are capable of influencing intestinal transport, corticosteroids and aldosterone probably exert a prolonged, modest, controlling influence on salt and water absorption. They are likely to be important in situations where variation in colonic absorption occurs, such as in the rabbit, or in circumstances where salt depletion or salt overload are likely. There is modest evidence in favour of the possibility that the gastrointestinal hormones liberated locally after a meal limit the rate of absorption of salt and water at that time, perhaps to maintain the fluidity of luminal contents for digestion to occur. More rapid short-term regulation of salt and water absorption in localized areas of the intestine may be exerted by peptide secretions from the enteric nervous system and paracrine cells. Cholinergic and adrenergic effects on secretion and absorption respectively may be responsible for maintaining an overall balance, and there is reasonable evidence in favour of this view. There is also strong circumstantial evidence to support a role for VIP in intestinal secretion. VIP may also play a part in mediating secretory diarrhoea. A role for the large number of other neurotransmitters remains uncertain but it is likely that overall control is maintained by a combination of counter-balancing factors. Finally, under pathological circumstances, where damage to the intestine liberates such mediators of the inflammatory response as prostaglandins, histamine and bradykinin, intestinal secretion may occur and be responsible for the diarrhoea associated with these diseases.

Animals↗
PubMed2000

Pathophysiology of the intrahepatic biliary epithelium.

The intrahepatic bile duct epithelium modulates the fluidity and alkalinity of the primary hepatocellular bile from which it reabsorbs fluids, amino acids, glucose and bile acids, while secreting water, electrolytes and immunoglobulin A. The transport function of the intrahepatic biliary epithelium is finely regulated by a number of gastrointestinal hormones, neuropeptides and neurotransmitters that promote either secretion or absorption. The intrahepatic biliary epithelium appears to be a primary target in a broad group of chronic cholestatic disorders that represent an important cause of morbidity and mortality. The spectrum of cholangiopathies ranges from conditions in which a normal epithelium is damaged by disordered autoimmunity, infectious agents, toxic compounds or ischaemia, to genetically determined disorders arising from an abnormal bile duct biology, such as cystic fibrosis or biliary atresia. Probably as a result of the known heterogeneity in cholangiocyte function, different portions of the biliary tree appear to be preferentially affected in specific cholangiopathies. From a pathophysiological point of view, cholangiopathies are characterized by the coexistence of cholangiocyte loss (by apoptotic or lytic cell death) with cholangiocyte proliferation and various degrees of portal inflammation, fibrosis and cholestasis. These basic disease mechanisms are discussed in detail. Better understanding of cholangiocyte pathophysiology, in particular the immune regulation of cholangiocyte function, will help in designing newer genetic or pharmacological approaches to treat cholangiopathies.

Absorption↗
PubMed1980

Serum motilin in gastrointestinal diseases.

In order to investigate the possible involvement of gastrointestinal hormones in functional disorders of the digestive tract, serum motilin, neurotensin and gastrin levels in their response to oral intake of fat and glucose were examined in patients with irritable colon syndrome and dumping syndrome. The following results were obtained. (1) Basal serum motilin levels were higher in patients with irritable colon syndrome than in normal subjects, and remained high after ingestion of either 50 g of butter or 50 g of glucose. (2) No consistent response in serum neurotensin levels was found in patients with irritable colon syndrome or in normal subjects. (3) An immediate increase in serum gastrin levels was found in response to fat ingestion both in patients with irritable colon syndrome and in normal subjects, but there was no difference between these two groups. (4) In a patient with typical dumping syndrome, a markedly high level of fasting serum motilin was found, and the level increased further after the oral intake of glucose. These findings suggest that motilin may be involved in the irritable colon syndrome and dumping syndrome.

Adult↗