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At least 811 records · Page 45Linked to original sources
PubMed1996

Effects of growth factors and gut hormones on proliferation of primary cultured gastric mucous cells of guinea pig.

Almost completely homogenous gastric mucous epithelial cells of guinea pigs were grown to confluence in the presence of 10% fetal calf serum (FCS). FCS, epidermal growth factor (EGF), and insulin significantly increased 5-bromo-2'-deoxyuridine (BrdU) uptake by the cells and EGF together with insulin increased the cells' [3H] thymidine uptake. Basic fibroblast growth factor (bFGF) enhanced EGF-induced DNA synthesis by the cells, but vasoactive intestinal peptide (VIP), secretin, prostaglandin E2 (PGE2), and dibutyryl cyclic AMP (dbcAMP) neither induced DNA synthesis nor enhanced the effect of EGF on DNA synthesis by the cells. Gastrin, cholecystokinin-octapeptide (CCK8), and carbamylcholine chloride (CCh) also did not enhance the effect of EGF on DNA synthesis. 125I-EGF, 125I-bFGF, and 125I-gastrin binding to the gastric mucous cells revealed the presence of high-affinity receptors for EGF and bFGF, but not for gastrin. Northern blot analysis showed the expression of EGF receptor mRNA, but not gastrin receptor mRNA. These results suggest that EGF, insulin, and bFGF may cooperatively regulate gastric mucous cell growth, but that gastrin and other gastrointestinal hormones do not have a direct stimulatory effect on mucous cell growth in the guinea pig.

Animals↗
PubMed1994

Effects of jejunoileal autotransplantation on gastrointestinal regulatory peptides.

Plasma gastrointestinal hormones were measured before and during feeding in eight dogs, more than one year after total autotransplant of the entire jejunoileum, and in controls. At sacrifice, tissues were taken from the transplanted segment and intact bowel for measurement of hormone and enteric neuropeptide content. Gastrin levels were reduced in autotransplanted dogs (fasting 63% of control, incremental response 67% of control, both P < 0.05), reflecting the loss of acid inhibitory reflexes. Secretin and cholecystokinin responses were identical between the two groups. Postprandial levels of gastric inhibitory peptide (incremental response 175% of control, P < 0.005), insulin, and peptide YY (158% of control, P < 0.05) were elevated following denervation, the former suggesting more rapid gastric emptying while the latter may reflect malabsorption. The neurotensin meal response was obtunded by denervation (incremental response 43% of control, P < 0.05), providing evidence for a neural pathway for its release. Pancreatic polypeptide responses were identical between the groups, suggesting intact pancreatic innervation. Abnormal hormone secretion may contribute to the impaired fed motor responses seen following extrinsic denervation of the small bowel. In contrast, the neuropeptide content of the autotransplanted small intestine is normal, suggesting that extrinsic denervation has no long-term effects on peptide content of the enteric nervous system.

Animals↗
PubMed1998

[The Studer orthotopic ileal neobladder: patient compliance].

Radical cystectomy represents the gold standard for locally advanced bladder cancer. Orthotopic neobladder is considered the surgical option which may offer the least modification of body image and the best life condition to the unfortunate patient requiring radical cystectomy. Objective of this study was to investigate long term clinical outcome of orthotopic ileal bladder substitute with special reference to late complications and patient compliance. Twenty male patients 48 to 71 years old (mean age 59.8 + 7.4 years) underwent radical cystectomy and Studer orthotopic ileal neobladder for invasive carcinoma of the bladder. Before surgery all patients filled in a phycometric test for evaluating their knowledge capacity; after surgery they underwent a course of biofeedback and instructed to avoid overfilling of the neobladder with timed micturitions and a regular regimen of fluid intake. Pressure flow study was included in the routine follow-up carried out at six months and then yearly. Seventeen patients (85%), with a good knowledge capacity, reported a good compliance to the modified life style imposed by the bladder substitute, they all were dry during the day with 3 to 5.5 hour interval between micturitions; fourteen of these patients were continent at night with timed micturitions every 3-4 hours (mean: 3.2); an average cystometric capacity of 450 ml was found in these patients with no residual urine; three patients (18%) had incontinence episodes once or twice a week during the night; no decompensation of the neobladder, significant ureteral reflux or dilatation were reported; elongation of the afferent loop was found in one patient following small bowel resection for ileal volvulus. Three patients (15%), with a reduced knowledge capacity, who did not follow the suggested life style: fluid intake was irregular, micturitions were not timed during both day and night time, had residual urine larger than 400 ml. and incontinence episodes requiring pads; nevertheless no dilation of the upper urinary tract was found. Our experience suggests that careful compliance of patients to the new life style imposed by the orthotopic neobladder is of importance to avoid its decompensation. The possible causative role of gastrointestinal hormones such as enteroglucagon (EG) and peptide tyrosine-tyrosine (PYY) in the elongation of the afferent limb of the Studer neobladder is proposed. In conclusion, we believe that orthotopic ileal neobladder is an ideal surgical option on in the young, educated and cooperative patients.

Aged↗
PubMed1982

Serum gastrin and motilin in treated and untreated hyperthyroidism.

To study the gastrointestinal hormones in hyperthyroidism and the interrelations with the thyroid hormones, the preprandial serum gastrin and motilin were measured by radioimmunoassay in 104 patients before and after the treatments. The following results were obtained: 1) Serum gastrin concentration in hyperthyroidism was significantly higher than that of the control, and when the patients reached euthyroidism or hypothyroidism after the treatments, the gastrin concentrations in the serum decreased to the normal level. There was a positive correlation between the thyroid hormones and the serum gastrin. 2) Serum motilin concentration in hyperthyroidism was slightly lower than that of the control. As the patients reached the euthyroid or hypothyroid state after the treatments, an increasing tendency of motilin was observed, though the change was not significant. There was a slightly negative correlation in gastrin versus motilin and also in T4 versus motilin.

Adult↗
PubMed1991

[The characteristics of acid-formation regulation in the stomach of patients with rheumatic diseases].

The content of gastrointestinal hormones was studied in the blood of 116 patients with rheumatic diseases (rheumatism, rheumatoid arthritis, osteoarthrosis deformans). Comparison of obtained data with values of the gastric acid forming function and results of histological examination of the duodenal mucosa allowed to determine some pathogenetic mechanisms developing in gastroduodenal complications which is a basis for rational treatment.

Arthritis, Rheumatoid↗
PubMed2003

Peripheral signals in the control of satiety and hunger.

PURPOSE OF REVIEW: Food intake is critical for survival and is a complex behavior with multiple levels of control. Short-term, meal-related signals arise from many sources including the gastrointestinal tract, the environment, and higher centers in the brain. As described in this review, inputs from the gastrointestinal tract can exert potent effects on meal initiation, meal termination, and meal frequency. The complex array of signals generated from the gastrointestinal system and from adipose tissue, which participate in the regulation of food intake, and specifically how these signals relate to satiety and hunger, is the focus of this review. RECENT FINDINGS: Literature on the role of the well-studied gastrointestinal peptide, cholecystokinin, in satiety, in addition to its interaction with long-term adiposity signals in mediating food intake will be reviewed. In addition, literature on the gastrointestinal hormones glucagon-like-peptide 1, apolipoprotein A-IV and peptide YY, and how they may act to regulate satiety, is described. Finally, the newly discovered hormone, ghrelin, and how it relates to meal initiation and hunger is discussed. SUMMARY: A better understanding of these systems and how they relate to body adiposity will prove to have important clinical applications. The available data suggest that interventions directed at multiple targets in the energy homeostasis system may be necessary to achieve and maintain weight loss.

Adipose Tissue↗
PubMed1983

[Participation of the gastrointestinal tract in regulating the processes of insulin liberation by the pancreas].

Three elevations of the insulin concentration in the blood of the v. pancreaticoduodenalis and v. portae were found in dogs fed with food containing mainly proteins, fat or carbohydrates. The gastrointestinal tract was found to potentiate the liberation of insulin. The elevation of the latter concentration in the blood occurred before the intensive absorption of the nutrients aided to, apparently, by liberation of some gastrointestinal hormones (gastrin, cholecystokinin-pancreozymin, GIP and others) which prepare the tissues for the assimilation of nutrients. A later elevation of the insulin concentration in the blood is possibly connected with absorption of aminoacids and some other nutrients and/or liberation of GIP in the small intestine.

Animal Nutritional Physiological Phenomena↗
PubMed1984

The gastrointestinal tract as an endocrine organ.

During the past several years gastrointestinal endocrinology has expanded its scope. Several specific clinical syndromes can be directly ascribed to abnormalities in the control of the gastrointestinal hormones. New concepts interrelating the gut and the brain have served as a stimulus for investigation of the interactions among control mechanisms in all aspects of human biology. The rapid, almost explosive progress in this area has been spearheaded by surgical physiologists, for which Dr. Graham would have been justly proud. Finally, it is important to spotlight the role that Washington University researchers have played in this developmental process.

Animals↗
PubMed1991

Response of the antral mucosa of the rat stomach to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) produces a striking hypergastrinemia in rats that is thought to mediate the antiatrophy effect of TCDD on the oxyntic gland mucosa of the stomach. However, effects of TCDD on the antral mucosa, which is the origin of most physiologically released gastrin and is not a target for the trophic action of gastrin, has yet to be thoroughly investigated. Also gastrin release from gastrin-containing cells (i.e., G-cells) in the antral mucosa is inhibited by the paracrine secretion of somatostatin from D-cells in the antrum. Our purpose was to determine if the antral mucosa is affected by the trophic influence of TCDD and if alterations in antral mucosa levels of gastrin or somatostatin cause the hypergastrinemia. TCDD (100 micrograms/kg, Day 14 post-treatment) had a trophic effect on the antral mucosa. This was demonstrated histologically and by significant increases in antral wet weight and antral mucosa height. In contrast, pair-fed control rats that lost the same amount of body weight developed antral mucosa atrophy. With respect to serum and antral levels of gastrointestinal hormones, TCDD produced a 7- to 10-fold increase in serum gastrin concentrations that was not detected until Day 14 post-treatment. In contrast, serum gastrin concentrations in pair-fed control rats were comparable to those of control rats. The number of G-cells in the antral mucosa was not affected by either TCDD treatment or paired-feed restriction. These findings demonstrate that hypergastrinemia in TCDD-treated rats is not caused by reduced feed intake or antral G-cell hyperplasia. A major finding was that antral mucosa levels of both gastrin and somatostatin were decreased significantly in TCDD-treated rats. However, the temporal development and dose-dependence of these TCDD effects on antral hormone levels were quite different than those for hypergastrinemia. TCDD-induced decreases in antral levels of gastrin and somatostatin were detected 1 week earlier than hypergastrinemia. Also, the ED50 of TCDD on Day 14 post-treatment for the decrease in antral mucosa content and concentration of gastrin (29 and 22 micrograms/kg, respectively) and somatostatin (24 and 19 micrograms/kg, respectively) was less than that for hypergastrinemia (46 micrograms/kg). These time- and dose-dependent differences demonstrate that hypergastrinemia in TCDD-treated rats is not a consequence of reduced antral levels of gastrin or somatostatin. We conclude that the antral mucosa, an epithelial tissue not responsive to the proliferative effect of gastrin, is nevertheless a target for the trophic influence and gastrointestinal hormone-altering effects of TCDD.

Animals↗
PubMed1982

Radioimmunoassay for vasoactive intestinal polypeptide (VIP) in plasma before and during endoscopic examinations.

A specific and sensitive radioimmunoassay of human vasoactive intestinal polypeptide using synthetic VIP as standard preparation and antiserum to synthetic VIP R 502 (Yanaihara et al. 15) is described. No crossreactions with a number of other gastrointestinal hormones such as glucagon, secretin, GIP, HPP or substance P was detected. Aprotinin (Trasylol, Bayer) or heparin had no influence on the antigen--antibody reaction. High concentrations of sodium or potassium chloride in plasma, or hyperlipoproteinemia, did not interfere with the antiserum in the described system. Basal plasma concentration of VIP in 18 females (means +/- sem = 24.05 +/- 1.79 VIP/l) and 20 males (means +/- sem = 24.11 +/- 1.91 pmol/l VIP) showed no sex specific variations. During gastroscopy plasma VIP levels were significantly higher than basal values, showing a peak secretion when the gastric antrum was inspected. During the entire colonoscopic examination, VIP levels were significantly higher than basal values. Endoscopic examination may possibly liberate VIP from the VIP containing cells which can be found throughout the gastrointestinal tract.

Adolescent↗
PubMed1981

Discrepant performance on oral and intravenous glucose tolerance tests: the role of gastric inhibitory polypeptide.

Analysis of a large study population revealed a group of eight healthy men whose tolerance to oral glucose was markedly greater than their tolerance to iv glucose (disparate group). The physiological basis of the anomalous performance was investigated using a variation of the hyperglycemic glucose clamp technique. This technique allows separation of the effects of hyperglycemia and intestinal insulinotropic factors on B-cell response. The eight subjects with disparate tolerance tests were compared to eight healthy control subjects whose tolerances on the two tests were very similar. The disparate performers showed 1) higher basal circulating gastric inhibitory polypeptide (GIP) levels, 2) lower immunoreactive insulin (IRI) responses to hyperglycemia (iv glucose alone), 3) enhanced GIP response to oral glucose, and 4) enhanced IRI response to oral glucose. These results may be interpreted as indicating a role for GIP in the improved tolerance for oral glucose, although other unknown gastrointestinal hormones could theoretically also be involved. Enhanced release of GIP after oral glucose may compensate for the reduced IRI release in response to hyperglycemia. The mechanism underlying the enhanced GIP response in these studies remains to be explored. It will be of interest to follow these subjects to see whether their anomalous gut beta-cell balance has any long term pathogenetic implications.

Administration, Oral↗
PubMed1996

The relationship between gut hormone secretion and gastric emptying in different phases of the migrating motor complex.

BACKGROUND: No studies are available on the relationship between the response of gut hormones and gastric emptying in different phases of the migrating motor complex. This study examined whether basal gut hormone concentrations in plasma before food ingestion are predictors of emptying characteristics and whether different hormone secretion patterns are associated with specific alterations in emptying rate. METHODS: Twelve healthy men were examined on two occasions: one with meal ingestion in phase I and the other with meal ingestion in phase II. The meal consisted of an omelette labelled with 99mTc followed by 150 ml water labelled with 111In. Plasma concentrations of gastrin, cholecystokinin, motilin, and peptide YY were measured in the fasting state, immediately after food ingestion, and at 15-min intervals in the postprandial period. RESULTS: New findings from the present study include a higher incremental integrated postprandial motilin response in phase I than in phase II (998 pmol/l*30 min (495 to 2010) versus 210 pmol/l*30 min (-270 to 2323), p < 0.05), and a linear relationship between median total integrated motilin response and solid emptying at 120 min in phase I (Rs = 0.58; p < 0.05). Furthermore, in phase I a linear relationship between total integrated area of cholecystokinin and solid emptying at 120 min was demonstrated (Rs = 0.62; p < 0.05). CONCLUSION: The findings from the present investigation have to be considered in the future design of studies that focus on postprandial release of gastrointestinal hormones. The transition from phase III to phase I is a reproducible and easily recognized pressure event. Therefore, we recommend the use of food ingestion immediately after termination of duodenal phase III.

Adult↗
PubMed1976

Syntheses of motilin analogues.

According to a first suggestion for the primary structure of the gastrointestinal hormone motilin, two analogues containing norleucine and leucine instead of methionine in the sequence position 13 (primarily called 13-norleucine and 13-leucine-motilin) have been synthesized. Both synthetic peptides were biologically active in equivalence to the natural product. A correction of the proposed amino acid sequence became necessary after rechecking the results by comparison with the synthetic materials. The two analogues must therefore correctly be named 13-norleucine-14-desamidomotilin and 13-leucine-14-desamido-motilin.

Amino Acid Sequence↗
PubMed1989

Cardiovascular, biochemical and hormonal changes during food-induced hypotension in chronic autonomic failure.

The cardiovascular, biochemical and hormonal responses to a standard test meal have been investigated in patients with chronic autonomic failure and normal subjects. In autonomic failure there was a rapid (within 15 min), substantial and prolonged fall in blood pressure after the meal. A marked fall in blood pressure also occurred after a liquid meal of similar composition and caloric content, with no change in blood pressure in age-matched subjects with normal autonomic function. In autonomic failure after the test meal the blood pressure reached its nadir (45% fall) after 60 min, and had not returned to pre-meal levels after 3 h. There were no changes in cutaneous and forearm blood flow. In the normal subjects there were no changes in blood pressure after the meal; forearm blood flow fell and cardiac output increased. In autonomic failure there were no changes in plasma noradrenaline levels, unlike the normal subjects. Plasma adrenaline levels were unchanged in both groups. There was a similar rise in levels of plasma renin activity in both groups. The haematocrit and plasma osmolality did not change in either group. Changes in plasma glucose and plasma insulin levels were similar in both groups. The responses of 3 pancreatic gut peptides, neurotensin, pancreatic polypeptide and enteroglucagon, were greater in autonomic failure. Basal levels and responses of vasoactive intestinal polypeptide, cholecystokinin-8 and somatostatin were similar in both groups. The motilin response was greater in normal subjects. We conclude that in patients with autonomic failure there was a rapid, substantial and prolonged fall in blood pressure after a meal. This reduction in blood pressure was not counteracted by an increase in sympathetic nervous activity and other compensatory changes, as occur normally. It was unlikely that osmotic effects of the meal or gut secretions resulted in a significant loss of intravascular fluid into the gut. The fall in blood pressure probably results from vasodilatation within the splanchnic circulation, to which pancreatic and gastrointestinal hormones with vasodilatory actions may contribute.

Adult↗
PubMedDate not supplied

Cholecystokinin receptors mediate enhanced memory retention produced by feeding and gastrointestinal peptides.

Ingestion of food in mice following training on T-maze footshock avoidance enhanced memory retention when tested 7 days later. This eating-induced improvement of retention was blocked by a specific cholecystokinin antagonist, L-364,718. The cholecystokinin antagonist prevented enhancement of memory retention resulting from posttraining administration of the gastrointestinal hormones, cholecystokinin, bombesin or gastrin releasing peptide. L-364,718 neither impaired or improved retention when given alone. Specificity of the effect of L-364,718 was demonstrated by the failure of L-364,718 to block improved memory retention resulting from administration of arecoline and D-amphetamine. The studies provide evidence that activation of cholecystokinin receptors plays a physiological role in the mediation of meal-induced enhancement of memory retention.

Animals↗
PubMedDate not supplied

Glucose-dependent insulinotropic polypeptide as a regulator of beta cell function and fate.

Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone that is secreted in response to food intake and modulates beta cell function. It may also regulate beta cell fate. Released from the nutrient-sensing K-cells of the upper intestine, GIP acts on various tissues, including pancreatic beta cells, via interaction with its G-protein-coupled receptor. Perhaps the most important effect of GIP is its potentiation of insulin secretion. Indeed, pharmacological blockade or genetic knockout of its receptor delays glucose-dependent insulin secretion. Exposure to GIP also enhances the beta cell response to future nutrient stimulation and upregulates transcription of key beta cell genes. There is emerging evidence that like the related hormone glucagon-like peptide-1, GIP may function as a beta cell growth factor and anti-apoptotic agent, further supporting a role for this hormone in balancing beta cell function to changing metabolic conditions. Overproduction of GIP in response to increased nutrient loads may, however, contribute to the pathophysiology of obesity. Interestingly, its insulinotropic effect is lost in type 2 diabetes, perhaps because of hyperglycemia-induced receptor desensitization. A better understanding of GIP's effects on the beta cell under normal and pathological conditions may facilitate the design of GIP derivatives for the treatment of metabolic disorders.

Apoptosis↗
PubMed1979

The incretin concept today.

1. The insulinogenic factor of the gastrointestinal mucosa named "incretin" is only one part of the complex enteroinsular axis. --2. Of the chemically defined gastrointestinal hormones GIP is the strongest incretin candidate. --3. Because of the dual function of GIP as gastrone and insulinotropic substance several safeguards against GIP-mediated insulin hypoglycaemia exist. --4. No pathological condition has yet been found which is causally related to hyper- or hyposecretion of GIP. However, an exaggerated GIP response (usually secondary to the disease) may participate in the pathogenesis of hyperinsulinaemia of patients with obesity and duodenal ulcer. --5. The injection of GIP antibodies only partially abolishes the incretin effect. Therefore, GIP, although important, is not the only incretin.

Absorption↗
PubMed2002

Potential of surgery for curing type 2 diabetes mellitus.

OBJECTIVE: To review the effect of morbid obesity surgery on type 2 diabetes mellitus, and to analyze data that might explain the mechanisms of action of these surgeries and that could answer the question of whether surgery for morbid obesity can represent a cure for type 2 diabetes in nonobese patients as well. SUMMARY BACKGROUND DATA: Diabetes mellitus type 2 affects more than 150 million people worldwide. Although the incidence of complications of type 2 diabetes can be reduced with tight control of hyperglycemia, current therapies do not achieve a cure. Some operations for morbid obesity not only induce significant and lasting weight loss but also lead to improvements in or resolution of comorbid disease states, especially type 2 diabetes. METHODS: The authors reviewed data from the literature to address what is known about the effect of surgery for obesity on glucose metabolism and the endocrine changes that follow this surgery. RESULTS: Series with long-term follow-up show that gastric bypass and biliopancreatic diversion achieve durable normal levels of plasma glucose, plasma insulin, and glycosylated hemoglobin in 80% to 100% of severely obese diabetic patients, usually within days after surgery. Available data show a significant change in the pattern of secretion of gastrointestinal hormones. Case reports have also documented remission of type 2 diabetes in nonmorbidly obese individuals undergoing biliopancreatic diversion for other indications. CONCLUSIONS: Gastric bypass and biliopancreatic diversion seem to achieve control of diabetes as a primary and independent effect, not secondary to the treatment of overweight. Although controlled trials are needed to verify the effectiveness on nonobese individuals, gastric bypass surgery has the potential to change the current concepts of the pathophysiology of type 2 diabetes and, possibly, the management of this disease.

Biliopancreatic Diversion↗