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At least 1,135 records · Page 63Linked to original sources
PubMed1985

Plasma motilin concentration and interdigestive migrating motor complex in diabetic gastroparesis: effect of metoclopramide.

The objective of this study is to determine whether abnormal rhythm and amplitude of the oscillation in plasma motilin concentration are responsible for the abnormal motility observed in patients with diabetic gastroparesis. We also investigated the effect of metoclopramide on plasma motilin concentration and gastrointestinal motility in these patients. In healthy controls, basal plasma motilin concentration fluctuated in phase with the interdigestive migrating motor complex. All patients with diabetic gastroparesis did not have antral phase III activities and had significantly higher basal motilin concentrations, which maintained a normal oscillatory pattern. Administration of metoclopramide initiated antral phase III activities in healthy controls and in patients with diabetic gastroparesis. These were accompanied by a concurrent rise in plasma motilin concentration in healthy controls, contrasting with a fall in plasma motilin concentrations in patients with diabetic gastroparesis. We conclude that diabetic gastroparesis is associated with absence of antral interdigestive migrating motor complex and with elevated plasma motilin concentration with normal cyclic fluctuations. Our studies also show that metoclopramide initiates antral phase III activities in diabetic gastroparesis independent of plasma motilin concentration.

Adolescent↗
PubMed1986

Familial visceral neuropathy with autosomal dominant transmission.

This report describes a family with a visceral neuropathy without extraintestinal manifestations transmitted over at least four generations in an autosomal dominant manner. Four of 7 living patients underwent extensive evaluation including histology, radiography, gastric emptying and secretory studies, esophageal and jejunal manometry, and measurements of plasma levels of gastrointestinal hormones. The only characteristic radiologic abnormality in 7 patients was dilatation of jejunum and ileum. Gastric emptying studies were normal in 2 patients, whereas 2 others showed accelerated emptying of liquids either alone or in combination with grossly delayed solid emptying. Manometry of the esophagus and proximal small intestine and gastric secretory studies were normal. Histologic studies showed hypertrophy of the smooth muscle, a markedly reduced number of argyrophilic neurons, and degenerative changes of argyrophilic neurons and nerve fibers but without Schwann cell proliferation, intranuclear inclusions, or inflammatory cells. This appears to be a familial visceral neuropathy characterized by distinct involvement of the jejunum and ileum as defined radiographically, histology different from that of two previously described forms of familial visceral neuropathy, autosomal dominant transmission, and no evidence for extraintestinal neurologic manifestations.

Adult↗
PubMed1987

Plasma levels of gastrin, somatostatin, and cholecystokinin immunoreactivity during pregnancy and lactation in dogs.

Plasma levels of gastrinlike, somatostatinlike, and cholecystokininlike immunoreactivity were determined by radioimmunoassay in peripheral blood from 11 beagles during pregnancy and in response to suckling during lactation. Cholecystokinin was determined in pooled and in individual plasma samples after separation of cholecystokinin and gastrin by high-performance liquid chromatography. Gastrin and somatostatin levels were significantly increased during the 8-wk-long dog pregnancy; peak values were recorded in week 7 and week 4, respectively. The cholecystokinin level rose and peaked at week 3, and remained elevated. In response to suckling, maternal gastrin levels rose significantly when tested in week 1 and 3 of lactation. Somatostatin levels did not respond significantly to suckling, but basal levels were elevated in week 1 compared to week 3 of lactation. Cholecystokinin rose in response to suckling both in week 1 and 3 of lactation. We suggest that the increased levels of gastrointestinal hormones during pregnancy and lactation may serve to increase digestive and anabolic capacity.

Animals↗
PubMed1988

Soy protein meals stimulate less gastric acid secretion and gastrin release than beef meals.

Soy protein is a widely used, inexpensive, and nutritious source of dietary protein. In contrast to beef protein, the effects of soy protein on gastric acid secretion and serum gastrin concentration have not been evaluated. We compared the effects of meals containing the same amounts of either isolated soy or beef protein on acid secretion and serum gastrin concentration in normal humans. Acid secretion measured by in vivo intragastric titration was 30%-40% less with soy than beef protein (p less than 0.05), whether isolated soy protein alone was compared with a mixed beef meal containing carbohydrate and fat or whether soy or beef meals containing similar amounts of fat were compared. Average gastrin rises were 65%-75% less with soy than with beef (p less than 0.01). The explanation for less gastrin release with soy than with beef is unclear, but lower serum gastrin concentrations with soy probably accounted for reduced acid secretion. These results indicate that the source of dietary protein in a meal may be an important determinant of gastric acid secretion and gastrointestinal hormone release.

Adult↗
PubMed1991

Mechanism of action of peptide YY to inhibit gastric motility.

The pathway by which peptide YY inhibits upper gastrointestinal motility is largely unknown and prompted this investigation. Muscle tension and [3H]acetylcholine release studies were performed on isolated muscle strips and slices obtained from the guinea pig stomach. Peptide YY [0.1-1000 nmol/L; concentration of half-maximal effect (EC50), 6 nmol/L] caused concentration-dependent relaxation of longitudinally oriented muscle strips that was unaffected by hexamethonium but was blocked by atropine and tetrodotoxin, suggesting that the peptide inhibited postganglionic cholinergic neurotransmission. In addition, peptide YY (1 mumol/L) reduced by 42% +/- 6% electrically stimulated muscle contractions that were blocked by atropine and tetrodotoxin, providing additional evidence that the peptide inhibits release of acetylcholine. Next, the effect of peptide YY on potassium-evoked release of [3H]acetylcholine and whether the peptide inhibits cyclic adenosine monophosphate-dependent release of acetylcholine were examined. Peptide YY (1 mumol/L) inhibited KCl (35 mmol/L)-evoked release of [3H]acetylcholine by 58% +/- 6%. The inhibitory action of peptide YY was unaffected by antagonists for dopamine-2, alpha-2, and opiate receptors that are known to mediate presynaptic inhibition. In addition, peptide YY reduced half-maximal forskolin and cholera toxin-evoked release of acetylcholine by 45% +/- 6% and 42% +/- 8%, respectively, suggesting that the peptide can inhibit cyclic adenosine monophosphate-dependent release of acetylcholine. This effect of peptide YY was reversed by pertussis toxin which prevents activation of the inhibitory guanine nucleotide binding protein coupled to adenylate cyclase. In summary, peptide YY inhibited basal and stimulated cholinergic neurotransmission in the guinea pig stomach. In addition, peptide YY antagonized cyclic adenosine monophosphate-mediated release of acetylcholine through a pertussis toxin-sensitive mechanism.

Acetylcholine↗
PubMed1995

Intraileal carbohydrate regulates canine postprandial pancreaticobiliary secretion and upper gut motility.

BACKGROUND & AIMS: The effect of nutrients in the distal small intestine or colon on postprandial upper gut function is incompletely understood. The aim of this study was to determine if carbohydrate in the ileum or proximal colon of dogs affects postprandial pancreaticobiliary secretion, gastrointestinal transit, and circulating concentrations of certain gastrointestinal regulatory peptides. METHODS: Seven dogs were prepared with permanent infusion and aspiration catheters in the duodenum and ileum and an infusion catheter in the cecum. Coincident with eating a meal containing liquid and solid markers, ileal or colonic (n = 5 dogs for each) infusion were begun of isosmolar 0.9% NaCl or carbohydrate in a 3:1 ratio of starch to glucose. Pancreatic enzyme output, bile acid delivery, gastrointestinal polypeptide, and plasma concentrations of pancreatic polypeptide, neurotensin, and peptide YY were measured for 6 hours postprandially. RESULTS: Carbohydrate infusion in the ileum, but not in the proximal colon, increased amylase secretion and plasma peptide YY, slowed gastric emptying of liquids and solids, slowed small intestinal transit, and decreased bile acid delivery into the duodenum (P < 0.05 in each). CONCLUSIONS: Carbohydrate in the ileum regulates postprandial exocrine pancreatic enzyme secretion and other postprandial upper gut functions. Peptide YY may play a role in this regulation.

Amylases↗
PubMed1990

Octreotide acetate induces fasting small bowel motility in patients with dumping syndrome.

The long acting somatostatin analogue octreotide acetate has been effective in the treatment of early dumping syndrome. We hypothesized that this may be related to its effects on inhibiting gastric emptying and delaying intestinal transit. To study the effect of octreotide acetate on intestinal motility in patients we carried out a randomized, double-blinded study using a subcutaneous injection of either octreotide acetate (100 micrograms) or placebo given 20 min prior to ingestion of a high carbohydrate "dumping" meal in six patients with known severe dumping syndrome. Prior to each study a multilumen polyethylene tube was inserted into the efferent limb to study small intestinal contractions using low compliance pneumo-hydraulic water-perfused manometry. Octreotide acetate prevented dumping symptoms in all six patients and induced the appearance of migrating myoelectric complexes (MMC) characteristic of interdigestive motility. After ingestion of the dumping meal the postprandial "fed" motility pattern lasted for 141 +/- 9 min while after octreotide acetate the fed motility lasted for 29 +/- 5 min (P less than 0.03). The vigor of the fed motility pattern as measured by the motility index (MI = loge (sum of amplitudes X No. of contractions + 1] was lower after octreotide acetate than after placebo (15.1 +/- 0.1 vs 13.4 +/- 0.2, P less than 0.03). The induction of fasting MMC motility pattern and reduction in the duration and vigor of fed motility may explain the symptomatic relief these patients obtained with octreotide acetate. It is not known whether the induction of the MMC is a direct effect of octreotide acetate or secondary to the concomitant inhibition of peptide release (neurotensin, insulin, glucagon, pancreatic polypeptide) that has been demonstrated in earlier studies.

Dumping Syndrome↗
PubMed1982

Vasoactive intestinal peptide causes peristaltic contractions in the esophageal body.

Vasoactive intestinal peptide (VIP) caused a dose-dependent fall in lower esophageal sphincter (LES) pressure and dose-dependent contractions in the body of the esophagus. The response to VIP in the esophagus or LES was not modified by atropine, phentolamine, haloperidol, pyrilamine, methysergide, indomethacin and tetrodotoxin, showing that is exerts direct action at the esophageal smooth muscle. These studies suggest that VIP causes contraction in the esophageal body and relaxation of the LES by a direct action on the smooth muscle. It is possible that VIP may be the common mediator of noncholinergic, nonadrenergic neurons that cause relaxation of the lower esophageal sphincter and contraction in the esophageal body.

Animals↗
PubMed1983

Direct modulation of epidermal growth factor binding by cholecystokinin.

The effects of cholecystokinin-octapeptide (CCK8), the biologically active C-terminal moiety of cholecystokinin (CCK), on the binding of epidermal growth factor (EGF) were studied in isolated rat pancreatic acini. CCK8 inhibited 125I-EGF binding in a dose-dependent manner. One-half maximal inhibition occurred at 5 X 10(-10)M, and maximal inhibition at 10(-8)M CCK8. This inhibitory effect was detectable within 5 minutes of addition of CCK8, and was not associated with enhanced degradation of 125I-EGF in incubation media. Unlabeled EGF exerted only a slightly greater inhibitory effect than CCK8 on 125I-EGF binding at equivalent molar concentrations. In contrast to CCK8, the gastrointestinal hormone vasoactive intestinal polypeptide (VIP) did not significantly alter EGF binding. CCK8 also inhibited EGF binding in mouse pancreatic acini, but did not alter binding in A-431 human carcinoma cells. These findings suggest that physiological levels of CCK may regulate EGF binding in the pancreas and other tissues with receptors for both hormones. They thus point to a previously unrecognized mechanism for hormonal interaction.

Animals↗
PubMed1983

Sites and mechanisms of action of neuropeptides on canine gastric motility differ in vivo and in vitro.

Motilin, pentagastrin and substance P (SP), injected intra-arterially into the canine gastric corpus in vivo increased the amplitude of contractions by an action dependent on activation of cholinergic nerves; i.e. atropine or tetrodotoxin (TTX) completely blocked the responses to motilin and pentagastrin and increased the ED50 of SP. TTX and atropine were not equally effective in increasing the ED50 for SP in vivo and the effect of combining them depended on the order of their addition. Both were much more effective than the SP analog D-Pro2, D-Trp7,9 SP (DSP) which appeared to be a weak antagonist of actions dependent on neural activity. In strips from the same region in vitro no receptors dependent on cholinergic nerve activation could be demonstrated for any peptide; i.e., all were atropine- and TTX-insensitive. Motilin, as expected in the absence of such receptors caused no contractile response in vitro. SP, also as predicted, caused contractions suggesting that a smooth muscle receptor, independent of nerve activation was present. However contrary to expectation pentagastrin induced an atropine and TTX-insensitive increase in the amplitude and frequency of contractions. These results show that 1) the most sensitive sites of action of a number of excitatory peptides depend on cholinergic nerve function in vivo; 2) such sites or the nerve activity on which they depend cannot be demonstrated in vitro; 3) SP has an additional site of action on smooth muscle demonstrable in vivo and in vitro, but motilin does not; 4) pentagastrin has only an action dependent on nerve function in vivo, but manifests an action independent of nerve function in vitro. We conclude that sites and mechanisms of action of peptides cannot be assumed to be identical in vivo and in vitro. Actions dependent on nerves are often lost in vitro and not all smooth muscle actions can be demonstrated in vivo.

Animals↗
PubMed1991

Disturbed cholecystokinin secretion in patients with eating disorders.

It has been shown that the gastrointestinal hormone cholecystokinin (CCK) induces satiety and reduces food intake in laboratory animals and humans. In the light of this evidence we studied CCK release in patients suffering from eating disorders. The secretion of CCK into the general circulation was measured in 10 anorectic, in 7 bulimic patients, and in 8 healthy controls before and after a high-caloric liquid testmeal. Baseline CCK values were similar in controls (0.6 +/- 0.2 pmol/l) and bulimics (0.6 +/- 0.1 pmol/l) and were significantly increased in the anorectic group (1.8 +/- 0.4 pmol/l) (p less than or equal to 0.005). After eating peak plasma levels increased to 6.1 +/- 0.9 pmol/l in the anorectic, to 3.8 +/- 0.5 pmol/l in the bulimic and to 2.7 +/- 0.6 pmol/l in the control group. All postprandial CCK values were significantly higher in the anorectic group. The secretion of CCK-8-S, an important peptide in the CCK family, was significantly elevated, too. This disturbed CCK secretion in patients suffering from anorexia nervosa, even if it is a secondary, diet-induced defect, may perpetuate this disorder.

Adolescent↗
PubMed1980

Therapy of insulin-independent diabetes mellitus: general considerations.

Rational approaches to the therapy of patients with insulin-independent diabetes should be based on correcting the underlying defects. The major metabolic abnormalities present in patients with insulin-independent diabetes are: (1) impaired insulin action, (2) defective glucose-mediated insulin secretion, and (3) hyperglucagonemia. All of these defects could be due to a generalized plasma membrane abnormality that affects insulin and glucose receptors or to a generalized disturbance in postreceptor insulin action. Insulin action may be increased by sulfonylureas, possibly by alterations in intracellular cyclic AMP content, or by weight-reducing diets. Insulin secretion may be increased by gastrointestinal hormones, sulfonylureas, serotonin antagonists, or weight-reducing diets. Individual patients with insulin-independent diabetes have varying degrees of insulin resistance or impaired glucose-mediated insulin secretion. The use of therapeutic agents to correct the predominant defect should provide the most effective means of controlling the hyperglycemia and glucose intolerance of the individual patient.

Blood Glucose↗
PubMed1993

Changes in plasma cholecystokinin concentrations after oral glucose tolerance test in anorexia nervosa before and after therapy.

There is considerable evidence that the gastrointestinal hormone cholecystokinin (CCK) induces satiety and reduces food intake in both animals and humans. Impaired CCK secretion was recently reported in patients with bulimia nervosa (BN) in whom plasma CCK responses to a standardized mixed-liquid meal were significantly lower than in controls. The present study was undertaken to determine whether CCK levels were abnormal in another relatively common eating disorder, anorexia nervosa (AN), before and after therapy and to investigate the relationship to the abnormal eating behavior. Plasma CCK, serum glucose, and immunoreactive insulin (IRI) responses to a 50-g oral glucose load were measured in 13 women with AN and in nine normal sex- and age-matched controls. The AN patients were all hospitalized during treatment; following partial restoration of body weight, the tests were repeated. Initial body weights were 70.8% +/- 1.8% (mean +/- SEM) of ideal body weight (IBW), and following partial restoration were 84.3% +/- 1.4%. Body weights in normal controls were 96.3% +/- 2.1% of IBW. Initial basal CCK concentrations in the AN patients before nutritional and cognitive behavioral therapy were significantly greater than those in controls (P < .01). After partial restoration of body weight, basal CCK concentration in AN patients approached that of control subjects. When AN patients were given a glucose load before therapy, the change in CCK response was diminished when compared with that of controls. However, CCK responses to the glucose load in AN patients following therapy were similar to those of controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1994

Reduced serum cholecystokinin response to food intake in female athletes.

Strenuous training in women has been shown to cause menstrual dysfunction and decreased bone mineral density. These endocrine and metabolic complications are associated with an insufficient dietary intake and decreased body fat content in female athletes. The present investigation was undertaken to study serum levels of cholecystokinin (CCK), insulin, gastrin, and cortisol in 14 female long-distance runners and 15 sex- and age-matched control subjects during intake of a standardized meal (500 kcal). The athletes showed a decreased response of the "satiety peptide" CCK to the meal and reported increased hunger compared with the control group. Meal-related insulin response was also decreased in the athletes, whereas gastrin levels were comparable to those of controls. Basal levels of glucose were increased in the athletes, but there was no difference in postprandial levels between the groups. Cortisol levels were clearly elevated in the female runners. We conclude that insufficient food intake in female athletes cannot be explained by increased CCK secretion and satiety. Since the athletes reported a larger caloric intake of a normal daily breakfast than the control subjects, the decreased CCK response may instead be explained by an adaptation to increased food intake. The decreased meal-related insulin response may be a reflection of increased insulin sensitivity as an adaptation to physical exercise. However, an impaired peptide secretion cannot be excluded. The role of elevated cortisol levels in the gastrointestinal hormone response needs further investigation.

Adult↗
PubMed1979

Cholecystokinin, amphetamine and diazepam and feeding in lean and obese Zucker rats.

The hyperphagia characteristic of some types of obesity may result from a deficiency in one or more components of the systems controlling satiety which in rats may include the gastrointestinal hormone cholecystokinin (CCK). Obesity may also influence responsivity to often used central nervous system (CNS)-acting drugs and combination of drugs. In these experiments it was shown that: (1) Zucker fatty rats were less sensitive than lean to intraperitoneal injections of 20 U/kg CCK after a 6-hr fast and when reduced were less sensitive than lean and less sensitive than when obese to injections of 5 U/kg CCK; (2) Although fatties were equally sensitive as leans to injections of 0.5 and 1.0 mg/kg d-amphetamine sulfate, when reduced, they were less sensitive; (3) Injections of 1.25 and 2.5 mg/kg diazepam produced smaller increases in food intake after a 6-hr fast in fatty and reduced fatty than lean rats; (4) Combination of diazepam with cholecystokinin in both fatty and lean rats produced feeding similar to that following injection of carrier; and (5) A similar additive effect was obtained in both fatty and lean rats when diazepam was combined with amphetamine; however, the fatty appeared to be more sensitive to the amphetamine than the diazepam effect. Thus the Zucker fatty rat appears to be less sensitive to these chemicals which affect food intake, which supports the contention that their CNS is generally less responsive.

Animals↗
PubMed1982

Pancreatic polypeptide is not involved in the regulation of the migrating motor complex in man.

The role of pancreatic polypeptide (PP) and motilin in the regulation of the migrating motor complex (MMC) was studied in normal subjects. Both plasma motilin and PP levels changed cyclically in the fasted state and were highest in the late phase II period preceding the activity front in the duodenum. A continental breakfast invariably disrupted the MMC and induced a fed pattern of motility. After the meal plasma motilin levels decreased whereas PP levels rose significantly. Infusion of pure porcine motilin during the fasted state induced an activity front and a rise in plasma PP levels. Infusion of bovine PP in doses producing plasma PP levels above the postprandial values neither induced an activity front nor prevented its occurrence. During PP infusion, however, plasma motilin levels were low, although the activity front was not inhibited. PP seems to have no clear role in the regulation of the motor component of the MMC of man. The role of motilin in the production of the activity front of the MMC is discussed.

Duodenum↗