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PubMed1983

[Incidence of peptic ulcer in diabetic disease: a clinic-epidemiological study].

We have investigated in 400 patients, 159 male and 241 female, mean age 58 years, with type 2 diabetes, the incidence of peptic ulcer and on 127 patients with peptic ulcer, the incidence of diabetes mellitus. In conclusion the incidence of peptic ulcer is no more than 3,9% in diabetic patients. In peptic ulcer the female to male ratio is 1:0,9. The seat of the ulcer is resulted to be in ratio of 1,4:1 more in the duodenal tract than in the gastric tract. The result are attributed to the increased secretion of the gastrointestinal hormones (Bombesin and Somatostatin) in the diabetic patients. However the neuromodulator of gastrointestinal hormones release is mediated of the Dorsal Motor nucleus of the Vagus nerve connected to the endocrine pancreas exclusively via vagal fibers and has a role in neurally mediated insulin release.

Adult↗
PubMed1996

Cardiovascular and hormonal responses to a meal in hypertrophic cardiomyopathy: a comparison of patients with and without postprandial exacerbation of symptoms.

Some patients with hypertrophic cardiomyopathy experience postprandial exacerbation of symptoms. The aim of this study was to determine whether the hemodynamic and/or hormonal responses to a meal differ between patients with and without postprandial symptoms. Ten hypertrophic cardiomyopathy patients with postprandial symptoms, 10 patients without postprandial symptoms, and 10 normal subjects ate a 740 Kcal meal, following which heart rate, blood pressure, and echocardiographic and gastrointestinal hormone changes were compared among the three groups. Heart rate increased (p < 0.001) and diastolic blood pressure fell (p < 0.001) to a similar degree in the three groups. Left ventricular outflow tract velocity increased (p < 0.01) and some patients had substantial increases in outflow tract pressure gradient; however, this was independent of the presence or absence of postprandial symptoms. The atrial contribution to filling increased in normal subjects and in both groups of hypertrophic cardiomyopathy patients. There was no significant difference in the gastrointestinal hormone changes in the three groups. In summary, there is no evidence for a distinctive hemodynamic or hormonal response to food in hypertrophic cardiomyopathy patients with postprandial symptoms. These symptoms more likely reflect differences in underlying cardiac disease characteristics and severity.

Adult↗
PubMed1994

Effects of dietary menhaden oil on mucosal adaptation after small bowel resection in rats.

BACKGROUND/AIMS: Adaptive hyperplasia of the small intestine is important in the outcome of short bowel syndrome. Previous studies have shown that long-chain fats stimulate this process. In the present study, the trophic effects of dietary menhaden oil, a highly unsaturated fat source, on mucosal adaptation following small bowel resection in rats was evaluated. METHODS: Thirty weanling Sprague-Dawley rats and their controls were fed diets containing fats provided primarily as menhaden oil, safflower oil, or beef tallow. After 4 weeks, animals underwent a 70% jejunoileal resection. Mucosal mass, DNA, protein, and sucrase levels were assessed 14 days after a 70% jejunoileal resection or control feeding. Serum fatty acid composition and several gastrointestinal hormone levels were measured. RESULTS: Resected animals fed menhaden oil showed a marked increase in mucosal weight, DNA, and protein levels compared with rats fed the other fat sources. Enteroglucagon level was increased in all resected groups, but least increased in the menhaden-fed animals. In contrast, peptide YY concentrations were most increased in animals fed menhaden oil. CONCLUSIONS: Menhaden oil appears more effective in inducing intestinal adaptation than less highly unsaturated fats. Analysis of gastrointestinal hormones revealed no clear-cut explanation for this finding, other than a modest but associated increase in peptide YY levels.

Adaptation, Physiological↗
PubMed1982

Pancreatic exocrine function in severe human chronic renal failure.

Patients with chronic renal failure have an abnormal immunoreactive gastrointestinal hormone profile, which is characterised by raised fasting serum concentrations of hormones that have antagonistic effects on exocrine pancreatic function. In addition, in this present study we have found that in renal insufficiency cholecystokinin disappears slowly from the plasma after a constant intravenous infusion of the hormone (p = 0.05 compared with healthy subjects). To evaluate whether the stimulatory or inhibitory hormones have a predominant effect, pancreatic exocrine function under conditions of mannitol perfusion of the duodenum and continuous intravenous cholecystokinin stimulation was studied in eight patients who had severe chronic renal failure and eight age-matched and sex-matched control subjects. Compared with healthy subjects, patients with renal insufficiency had hypersecretion of trypsin in response both to mannitol perfusion of the duodenum and to cholecystokinin stimulation (p less than 0.05). No significant differences in lipase secretion were noted between the patients with renal insufficiency and control subjects. These findings are consistent with the hypothesis that, of the abnormally raised fasting serum concentrations of gastrointestinal hormones found in renal insufficiency, hormones that stimulate rather than inhibit pancreatic exocrine function predominate. Secondly, the dissociation between trypsin and lipase outputs in chronic renal failure may suggest a differential trophic influence of stimulatory hormones -- that is, hypercholecystokininaemia -- on pancreatic exocrine enzyme secretion.

Adult↗
PubMedDate not supplied

[Checking of some hypotheses of the pathogenesis of diabetes mellitus by mathematical modeling].

A mathematical model of normal regulation of carbohydrate metabolism by the pancreas endocrine apparatus is presented. In a numerical experiment the model imitated changed levels of sucrose, insulin glucagon and gastrointestinal hormones in the blood in response to the ingested 50 g of glucose. The model of normal regulation was damaged in the way which theoretically should result in diabetes development. Then an estimation was made to what extent the disturbances of carbohydrate metabolism characteristic of diabetes were reproduced by the changed model. It has been shown that disturbances specific for diabetes appear when the sensitivity of beta-cells to glucose stimulus or hyperproduction of glucagon decreased. No changes in the behaviour of blood glucose typical of diabetes were obtained in the model when a decrease of the sensitivity of insulin receptors due to hyperinsulinemia in insulin-dependent tissues was imitated, as well as an increased activity of liver insulinase or hyposecretion of gastrointestinal hormones. These results point to the necessity of further development of these hypotheses.

Blood Glucose↗
PubMed1985

[Effect of subtotal small intestine resection on insulin and glucagon secretion by the isolated perfused rat pancreas following glucose stimulation].

An attempt has been made to investigate possible regulatory effects of gastrointestinal hormones on insulin and glucagon secretion in Wistar rats that had been subjected to partial resection of the duodenum and jejunum or the ileum. Release of insulin and glucagon was studied on perfused pancrease 4 weeks after the operation. Partial resection of both the duodenum and jejunum resulted in a significant decrease of glucose-induced insulin secretion and basal glucagon release when compared with the controls. Glucagon release was not further suppressed by increasing glucose concentration in the perfusion medium. Resection of the ileum only had no effects. Also, there was no difference to be observed in plasma insulin levels between the two groups. Resection of the ileum, however, provoked a drastical decrease of plasma insulin levels. Food intake was not significantly changed while body weight slightly decreased 1 week after operation but returned to normal after 4 weeks. The results suggest that the various parts of the small intestine seem to be involved in the regulation of glucose-stimulated insulin secretion as well as basal glucagon release. The alterations in glucose-stimulated insulin or glucose-suppressed glucagon secretion are likely due to the action of gastrointestinal hormones or hitherto unknown peptides.

Animals↗
PubMed1977

Pancreatic acinar cell metabolism and function.

This review outlines progress made during the past 11 years in research related to pancreatic acinar cell metabolism and function. We have reviewed information gained at the cellular level concerning structural and functional relationships, and effects of fasting and feeding, as well as the action of gastrointestinal hormones and cholinergic agonists on acinar cells. In toto, this information outlines a significant role for gastrointestinal hormones as mediators of secretion, synthesis, and control of trophism. This information provides a basis for more sophisticated inquiries as to the mechanisms of injury of alcohol and drugs. The information may prove helpful in developing diagnostic modalities for pancreatic disease, as well as understanding the processes involved in neoplastic transformation.

Amino Acids↗
PubMed1984

Stainability of the peptide hormones in gastrointestinal apudomas as demonstrated by immunoperoxidase kits.

A series of 25 apudomas of the gastrointestinal tract (22 cases), bronchus (2 cases), and thymus (1 case) were subjected to staining with silver impregnation (Masson-Fontana and Grimelius) techniques and with the commercial immunoperoxidase kits for the peptide hormones adrenocorticotropin, calcitonin, gastrin, glucagon, growth hormone, human chorionic gonadotropin (hCG), insulin, somatostatin, and vasoactive intestinal peptide. Of the tumors studied, 16 were regarded as malignant, and 5 of the patients showed clinical symptoms due to inappropriate hormone secretion. A total of 16 tumors contained cells positive for 1 or more (6 were multihormonal) of the hormones studied. One bronchial carcinoid stained for hCG, which has not been previously reported. In addition, one of the rectal carcinoids contained somatostatin-positive cells, only once described previously. The thymic tumor proved frankly malignant, most probably identical to the oat-cell carcinoma recently described. The findings also substantiate the recent suggestion that gastrointestinal carcinoids cannot be adequately classified on the basis of silver stains only and strongly advocate the use of the immunoperoxidase kits in routine assessments of all the endocrinologically active tumors, whatever their localization might be.

Adrenocorticotropic Hormone↗
PubMed2003

Octreotide abolishes the acute decrease in bone turnover in response to oral glucose.

Feeding or oral intake of glucose results in an acute suppression of bone turnover. This does not appear to be mediated by insulin. Several gastrointestinal hormones modulate bone turnover in vitro and may mediate this response. We examined whether inhibiting the production of gastrointestinal hormones using octreotide could block glucose-mediated suppression of bone turnover. Fifteen subjects were each studied on four occasions in a randomized, single-blind, crossover study after receiving 1) oral placebo, iv saline; 2) oral glucose, iv saline; 3) oral glucose, iv octreotide; or 4) iv octreotide alone. We measured serum C-terminal telopeptide of type I collagen, urinary N-terminal telopeptide of type I collagen, osteocalcin, procollagen type I N-terminal propeptide, PTH, insulin, ionized calcium, and glucose over 4 h. All bone turnover markers decreased significantly after oral glucose (P < 0.001). At 120 min serum C-terminal telopeptide decreased by 45 +/- 2%, urinary N-terminal telopeptide by 31 +/- 7%, osteocalcin by 16 +/- 1%, and procollagen type I N-terminal propeptide by 8 +/- 1%. There was no significant decrease in bone turnover in response to oral glucose during octreotide infusion. Octreotide alone resulted in a significant increase in all bone turnover markers (P < 0.05) and PTH (P < 0.01). We conclude that octreotide completely abolishes the bone turnover response to glucose intake and increases PTH secretion. The apparent bone turnover response to feeding is probably mediated by an octreotide-inhibitable endocrine factor.

Administration, Oral↗
PubMed1996

Biology of colorectal and gastric cancer cell lines.

Cell lines established from the human colorectal and gastric cancers may provide very useful tools to the study of the disease and to develop and test new therapeutic approaches, and a large bank of well-characterized cell lines should reflect the diversity of tumor phenotypes and provide adequate models for the study of tumor heterogeneity. Colorectal lines are relatively easy to establish, while gastric cancer cell lines remain extremely difficult to propagate in long-term culture, and the number of cell lines is very limited. In this paper, we describe the up-to-date results of the characteristics of our nine colorectal cancer cell lines and four gastric cancer cell lines. Based on culture, xenograft, and ultrastructural morphologies, these cell lines could be subtyped into well-differentiated, moderately differentiated, poorly differentiated, and mucinous carcinomas. Basic properties concerning expression and secretion of antigens, neuroendocrine features, receptor binding of various gastrointestinal hormones and neurotransmitters, cytogenetic studies, gene amplification and expression, and chemosensitivity profiles are described. In particular, a greater number of receptors for hormones and neurotransmitters are expressed on human colorectal cancer cell lines compared to gastric cancer cell lines, raising the possibility that gastrointestinal hormones may have a greater autocrine effect on colon cancer cell growth. Despite major differences in the biology of colorectal cancer and gastric cancer as indicated by clinical studies, the multiple properties that we examined reveals marked similarities between the colorectal and gastric cancer cell lines. However, in vitro chemosensitivity patterns to cytotoxic drugs are very different in colorectal and gastric cell lines. Some of these observations may be due to the relatively low expression of the multidrug-resistance-associated (MDR1) gene in gastric cancer cell lines. In addition, colorectal cancer cell lines express receptors for peptide hormones more frequently.

Adenocarcinoma↗
PubMed1988

Effects of bombesin and gastrin-releasing peptide on memory processing.

We have previously shown that feeding mice immediately following training enhances memory retention and that one of the gastrointestinal hormones released during a meal, cholecystokinin, also enhances retention after peripheral administration. In the studies reported here we demonstrate that another gastrointestinal peptide, gastrin-releasing peptide (GRP), enhances retention after peripheral administration, as does its amphibian counterpart, bombesin. GRP had the same effect as the intact peptide, while GRP was ineffective at enhancing retention. The dose-response curves showed a characteristic inverted U-shape with high doses of both GRP and bombesin being amnestic. The effect of both peptides was time-dependent and both reversed amnesia induced by the anticholinergic, scopolamine. I.c.v. administration of the peptides required higher doses to produce an effect on memory retention, suggesting that the effect was mediated predominantly through a peripheral mechanism. Doses of the peptides that enhanced memory retention after peripheral administration failed to increase serum glucose, suggesting that glucose modulation was not the mechanism by which GRP and bombesin modulate memory processing. Vagotomy inhibited the memory-enhancing effects of both GRP and bombesin, suggesting that these peptides produced their effect by stimulating ascending vagal pathways. These studies, together with our previous study with cholecystokinin, suggest the existence of a gastrointestinal hormonal system, which is activated by the passage of food through the intestine, that enhances memory retention.

Animals↗
PubMed1983

Effect of somatostatin, secretin, and glucagon on secretagogue stimulated aminopyrine uptake in isolated canine parietal cells.

Somatostatin, secretin, and glucagon have been shown to inhibit gastric acid secretion in vivo and thus have been postulated to act directly on the parietal cell. To test the hypothesis that these peptides directly influence the acid secretory cells, we studied the effect of the three gastrointestinal hormones using aminopyrine uptake as an index of acid production. The parietal cells were stimulated to increase aminopyrine uptake by submaximal concentrations of histamine (10(-6) mol/l), methacholine (10(-6) mol/l), and pentagastrin (10(-6) mol/l), but in no concentrations did these gastrointestinal hormones affect any of the secretagogues' response. Our data suggest that gastrointestinal peptides do not modulate acid secretion at the parietal cell level.

Aminopyrine↗
PubMed1994

Gastrointestinal peptide hormones during postoperative ileus. Effect of octreotide.

The hypothesis was that postoperative ileus might be caused by a disturbed balance between the motor-stimulating hormones, motilin and substance P, and the motor-inhibitory hormone, vasoactive intestinal polypeptide, and that octreotide might prevent this disturbance and so ameliorate the ileus. In 15 conscious dogs with chronic gastrointestinal electrodes, electrical activity was recorded and blood was drawn for radioimmunoassay of motilin, substance P, and vasoactive intestinal peptide (VIP) during fasting and after a liquid meal. Ileus was then induced by celiotomy and intestinal abrasion. During and after operation, five dogs received 154 mM NaCl only, five dogs octreotide, 0.19 micrograms/kg/hr, and five octreotide, 0.83 micrograms/kg/hr. Plasma levels of motilin, substance P, and VIP were changed little by operation, but cyclical increases in plasma motilin, which occurred preoperatively during phase III of the interdigestive myoelectric complex, were completely abolished postoperatively during ileus, as was the complex itself. Octreotide ameliorated the ileus and restored the cyclic increases in motilin found in health, nor did it alter plasma substance P and VIP. In conclusion, octreotide ameliorates postoperative ileus, but it does not do so by increasing plasma motilin or substance P or decreasing plasma VIP.

Animals↗
PubMed1979

Actions of thyrotropin-releasing hormone on gastrointestinal functions in man. III. Inhibition of gastric motility in response to distension.

The intragastric pressure/volume relationship has been measured in six healthy volunteers. Increased gastric motility was achieved by gastric distension, by stepwise increasing the volume from 0--600 ml. When thyrotropin-releasing hormone (TRH), 0.04 mg/h, was infused concomitantly in the individuals, gastric motility was significantly inhibited (p less than 0.05) and, with 1 mh/h of TRH, nearly abolished compared with the saline control test. The basal pressure was unaffected at 0.04 mg/h, whereas a significant rise was seen after 1 mg/h of TRH (p less than 0.05) compared with the control test. In three of the subjects the effect of rapid injection of TRH (0.2 mg), followed by infusion of TRH (0.6 mg/h), on the stimulated gastric motility was analysed. After the injection of TRH, almost no motor activity was observed during the 15-min observation period. It is concluded that TRH has a potent inhibiting effect on gastric motility, and the possible physiological role of TRH in the gastric regulation in man is discussed.

Adult↗
PubMed1999

Effect of feeding before, during and after milking on milk production and the hormones oxytocin, prolactin, gastrin and somatostatin.

Feeding during milking has been shown to influence milk production, milk flow and milking time as well as the secretion of the pituitary hormones oxytocin and prolactin, and the gastrointestinal hormone somatostatin. However, it is not known whether feeding before or after milking has any effect. The aim of the present study was to investigate how the timing of feeding relative to milking influences milk production and flow, milking time and hormone secretion. The trial was carried out over 9 weeks with 24 cows at varying stages of lactation. Each treatment period lasted for 3 weeks, including one registration week. The cows were fed ad lib. and were exposed to three treatments: feeding 1.5 h before milking (FBM), feeding at exactly the same time as milking (FDM) and feeding 1.5 h after milking (FAM). The most marked treatment effect was observed during morning milking. FDM resulted in higher milk production and higher yields of protein and lactose. FAM produced a lower fat yield and a lower fat content compared with FDM, and a lower lactose content than either FBM and FDM. Milking time was longer when cows were fed during milking, but no significant effects on milk flow were found. The amount of milk collected during the first 2 min of milking was lower when cows were fed after milking. Milking-related oxytocin and somatostatin secretion was lower in FAM than in FDM. The level of prolactin was lower when cows were fed before or after than during milking. More studies are needed to elucidate whether there is a long-term effect on milk production related to the discussed milking routines.

Animals↗