Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The gastric secretory effects of protein, fat, and carbohydrate infused at different levels of the small bowel were investigated in seven healthy subjects. Similar caloric loads (53.4 kcal) of protein (essential amino acids), lipid (oleic acid), and carbohydrate (glucose) in isomolar (280 mosmol/l) similar pH (7.4) solutions were infused into 60-cm segments of small bowel (isolated between two occlusive balloons), located distal to the ligament of Treitz (proximal), proximal to the ileocecal valve (distal), and between the two (middle). A submaximal gastric secretory background was provided by continuous intravenous pentagastrin. Protein stimulated acid secretion in the proximal (increase of 8.7 meq/h, representing 84 +/- 5% of control level) and middle (increase of 1.9 meq/h, representing 16 +/- 2% of control level) segments, while it inhibited acid secretion when infused into the distal segment (decrease of 3.7 meq/h, representing 33 +/- 4% of control level). In contrast, both lipid and carbohydrate inhibited acid secretion similarly (33-38% of control level) at all levels of the bowel. The different effects of protein at different levels of the bowel could not be explained by differences in serum gastrin, different degrees of absorption, or different postabsorptive levels of alpha-amino nitrogen. This suggests the presence of hormonal (nongastrin) or neural mechanisms in the proximal bowel to stimulate acid secretion and/or in the distal bowel to inhibit acid secretion. Thus, factors that determine specific nutrient loads to specific segments of bowel can have important physiological effects on gastric acid secretion.
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PMID:Nutrient and bowel segment dependency of human intestinal control of gastric secretion. 713 54

This study examined the effects of eradication of Helicobacter pylori (H pylori) infection on gastric mucosal morphology and acid secretion. Sixteen H pylori positive patients with enlarged gastric body folds were divided into two groups: (a) patients with moderate enlargement (fold width: 6 to 10 mm, n = 8) and (b) patients with severe enlargement (> 10 mm, n = 8). After successful treatment, gastric body fold width was reduced in both groups (p < 0.01) with an associated decrease in inflammatory infiltrates in the body mucosa (p < 0.01 and p < 0.05). Basal acid output and tetragastrin stimulated maximal acid output (mean (SEM)) in all 16 patients significantly increased from 1.1 (0.5) to 2.9 (0.9) mmol/h (p < 0.05) and from 5.4 (1.3) to 18.7 (2.3) mmol/h (p < 0.01), respectively, with a significant decrease in fasting serum gastrin concentrations, from 127.1 (16.1) to 59.6 (3.8) pg/ml (p < 0.01). The increase in acid secretion after eradication of H pylori was more noticeable in the severe group, who had shown lower acid secretion and higher serum gastrin concentrations (p < 0.05) before eradication, than the increase seen in the moderate group. The decreases in ammonia nitrogen content seen after eradication were significant in basal (from 0.91 (0.17) to 0.37 (0.08) mmol/h, p < 0.05) and stimulated gastric secretions (from 1.57 (0.19) to 0.37 (0.13) mmol/h, p < 0.01), although these changes were too small to explain the increases in basal acid output and maximal acid output. These results suggest that inflammation of the gastric body mucosa caused by H pylori infection is associated with enlarged gastric body folds and inhibition of acid secretion in H pylori positive patients with enlarged gastric body folds.
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PMID:Improved fold width and increased acid secretion after eradication of the organism in Helicobacter pylori associated enlarged fold gastritis. 782 75

Ostertagia spp. affect their hosts in several complex interactions involving structural, biochemical, hormonal, nutritional and immunological mechanisms. Following infection with Ostertagia spp. the specialised secretory function and junctional integrity of gastric epithelial cells is lost. The pH of the abomasal contents is elevated and pepsinogen concentration in the plasma increases. There is a concurrent elevation in the concentration of blood gastrin. The effects may be a response to the physical interaction of parasite with epithelial cells, may be mediated through parasite excretory/secretory products, or by neural mechanisms. There may also be interactions between the responses since elevated abomasal pH stimulates secretion of gastrin. Hormonal changes may also have a role in the increased susceptibility of host to parasite during the periparturient period. Prolactin was considered the most likely hormone candidate although there is now a body of evidence to suggest that elevated prolactin concentrations are not solely responsible. Infection with Ostertagia spp. causes a marked inappetance, negative nitrogen balance and reduction in apparent gross energy digestion. The level of nutrition may also affect the response of the host to the parasites and establishment of O. circumcincta is lower in animals on a low plane of nutrition than those on a high plane. Immunity of Ostertagia spp. develops slowly and once established is manifest following challenge by an initial hypersensitivity response, followed by a cell mediated response and then an antibody response. Parasites may fail to establish or may be expelled from immune animals and if they do establish may be stunted with small vulval flaps and lower biotic potential and may become inhibited at the early fourth stage of development.
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PMID:Interactions of Ostertagia species with their bovine and ovine hosts. 835 96

Infection with the abomasal nematode, Ostertagia ostertagi, is an important cause of impaired productivity in young cattle in temperate parts of the world. Such losses have been associated with marked changes in feed intake, gastrointestinal function, protein, energy and mineral metabolism, and in body composition. The reduction in feed intake is an important factor in the pathogenesis of infection and may account for a large part of the difference in weight gain between ad libitum fed control and infected calves. Despite the obvious importance of inappetance, only recently has an association been made between reduced intake, altered gut motility and elevated levels of certain gastrointestinal hormones, such as gastrin. It has been suggested that the elevated gastrin levels accompanying abomasal parasitism may impair reticulo-ruminal motility and slow down abomasal emptying, leading to a stasis of ingesta and a reduction in feed intake. The rise in blood gastrin levels may also be partly responsible for the marked hyperplasia of the fundic mucosa seen in abomasal infections. Pronounced changes in protein metabolism have also been associated with Ostertagia infection. Radioisotopic studies have demonstrated increased losses of albumin into the gastrointestinal tract which are accompanied by an increase in the rate of synthesis in the liver. Dietary protein breakdown in the abomasum is also likely to be impaired, although there is evidence of a compensatory increase in protein digestion in the lower gut of parasitised calves. Increased losses of albumin are not always accompanied by increases in faecal nitrogen, suggesting that albumin is broken down and recycled as ammonia. Radioisotopic studies in animals with intestinal nematode infections have demonstrated a marked reduction in muscle protein synthesis and an increase in protein synthesis in gastrointestinal tissue. Such changes in the balance of protein synthesis are likely to be brought about by alterations in the balance of certain metabolic hormones. Marked changes in energy metabolism also accompany Ostertagia infection. Parasitised calves exhibit a marked increase in non-esterified fatty acid levels, resulting from the mobilisation of adipose tissue, and a reduction in digestive efficiency of energy, probably associated with the increase in cycling of protein through the gastrointestinal tract and the compensatory increases in protein synthesis. Mineral metabolism may also be affected although relatively little work has been conducted in cattle. Changes in body composition reflect a reduction in deposition of muscle protein and fat, and an increase in bone content and water retention.
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PMID:Pathophysiology of infection with Ostertagia ostertagi in cattle. 848 7

Gastrectomy (GX) was carried out in the male rat according to the Longmire and the Roux-en-Y procedure. The focus of the postoperative investigations was to evaluate the influence of post-GX morphological changes occurring at the site of two types of end-to-end esophagojejunal anastomosis (with and without invagination), in particular food intake, body weight gain, food efficiency, hematocrit and bone density. GX failed to alter food intake, fasting blood glucose, alpha-amino nitrogen, or free fatty acids, but led to uniformly decreased body weight, food efficiency and serum gastrin, and increased serum osteocalcin, indicating high turnover osteopenia. However, irrespective of the type of (digestive tract) reconstruction (Longmire or Roux-en-Y), the invagination anastomosis was associated with lower mortality, fewer complications, less early postoperative weight loss, less intensive tissue changes at the anastomotic site, and improvement of bone density and hematocrit. Bivariate and multivariate regression analysis revealed that bone density was negatively influenced by epithelial hyperplasia of the anastomotic tissue, while hematocrit was positively influenced by bone density. In contrast, food intake appeared to have no influence. It was concluded that (1) the histological status of the esophagointestinal anastomosis varies depending on the surgical technique applied and (2) the type of anatomical reconstruction of the digestive tract (Longmire vs. Roux-en-Y) and food intake may be of minor importance for the bone and hematological status of GX rats. Future investigations are justified to clarify whether esophagojejunal proinflammatory tissue factors may contribute to the GX-mediated damage of bone mineral and bone marrow, thereby leading to low body weight.
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PMID:Gastrectomy in the rat using two modifications of esophagojejunal anastomosis. general status, local histological changes and relationships to bone density. 1086 46

Insulin-like growth factor-I (IGF-I) has been demonstrated to exert a nitrogen sparing effect, both experimentally and in patients after abdominal surgery. IGF-I is a major mediator for the anabolic effects of growth hormone (GH). Whether elevated circulating IGF-I levels are the sole mediator of the anabolic effects following GH has not been clarified. IGF-I influences glucose metabolism, both through its own specific receptor and by activating the insulin receptor, and has also been proposed to influence pancreatic islet secretion directly. In the present study, the postoperative effects of IGF-I on plasma levels of other gastrointestinal and pancreatic islet hormones and growth factors were measured in patients after abdominal surgery. Fifteen patients who were candidates for large bowel resection were randomly divided into two groups: IGF-I-treated (n=8) and placebo-treated (n=7). The IGF-I group received daily two s.c. injections of human recombinant IGF-I (80 microg/kg body weight) for five days, beginning on the morning of the first postoperative day. The other group received placebo injections. Fasting plasma levels of gastrointestinal growth factors (epidermal growth factor, transforming growth factor-alpha, IGF-II), gastrointestinal hormones (gastrin, enteroglucagon, peptide YY), and islet hormones (insulin, islet amyloid polypeptide (IAPP) and pancreatic glucagon) were determined by RIA preoperatively and after five days of treatment. No significant effects of IGF-I on other growth factors or gastrointestinal hormones were seen. A marked increase in plasma insulin postoperatively compared with the preoperative levels (42+/-3 vs 61+/-5 pM, P<0.05) was seen in the placebo group, whereas the postoperative levels in the IGF-I-treated patients remained unchanged (44+/-3 vs 45+/-4 pM). A similar pattern was observed for IAPP and cortisol concentrations. No differences in glucagon concentrations were seen. In conclusion, these results suggest that IGF-I does not influence production of other gastrointestinal hormones thought to be involved in alimentary growth or pancreatic glucagon. In contrast, IGF-I caused a marked reduction of insulin and IAPP secretion. The inhibition of beta-cell secretion could be direct or, alternatively, could involve an improvement in postoperative insulin resistance, perhaps by reducing serum cortisol.
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PMID:Gastrointestinal growth factors and pancreatic islet hormones during postoperative IGF-I supplementation in man. 1105 48

Early enteral support is believed to improve gastrointestinal, immunological, nutritional, and metabolic responses to critical injury; however, this premise is in need of further substantiation by definitive data. The purpose of this prospective study was to examine the effectiveness and safety of early enteral feeding in pediatric patients who had burns in excess of 25% total body surface area. Seventy-seven patients with a mean percent total body surface area burn of 52.5 +/- 2.3 (range 26-91), percent full thickness injury of 44.7 +/- 2.8 (range 0-90), and age ranging from 3.1 to 18.4 (mean 9.3 +/- 0.5) were randomized to two groups: early (feeding within 24 hours of injury) vs control (feeding delayed at least 48 hours postburn). Nutrient intake was measured daily, indirect calorimetry was performed biweekly, and blood and urine samples were obtained for the assay of cortisol, glucagon, insulin, gastrin, epinephrine, norepinephrine, dopamine, triiodothyronine, tetraiodothyronine, albumin, transferrin, prealbumin, retinol-binding protein, glucose, nitrogen balance, and 3-methylhistidine throughout the study period. Three protocol violations occurred, and two patients were transferred to another hospital; these patients were excluded from the study. No patient in either group experienced tube feeding aspiration. No differences were evident in infection, diarrhea, hospital length of stay, or mortality outcomes. A higher incidence of reportable adverse events coincided with early feeding (22 vs 8%), but this was not statistically significant. The delayed feeding group demonstrated a significant caloric deficit during postburn week (PBW) 1 (P <.0001) and PBW2 (P =.0022). Serum insulin (P =.0004) and triiodothyronine (P =.0162) were higher in the early fed group during PBW1. A decrease in 3-methylhistidine output (suggesting a decrease in protein breakdown) was also evident during PBW1 (P =.0138). No other significant trends in study outcome variables were noted. In conclusion, provision of enteral nutrients shortly after burn injury reduces caloric deficits and may stimulate insulin secretion and protein retention during the early phase postburn. These data, however, do not necessarily reaffirm the safety of early enteral feeding, nor do they associate earlier feeding with a direct improvement in endocrine status or a reduction in morbidity, mortality, hypermetabolism, or hospital stay. Future studies are needed to establish precise feeding implementation times that maximize clinical benefit while minimizing morbidity in the critically injured burn patient.
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PMID:The 2002 Clinical Research Award. An evaluation of the safety of early vs delayed enteral support and effects on clinical, nutritional, and endocrine outcomes after severe burns. 1243 17

A 59-year-old woman with chronic renal failure due to type 2 diabetes mellitus (DM) is presented. Her father and a brother had a history of brain tumor. Her blood urea nitrogen and serum creatinine levels were 102 mg/dl and 4.5 mg/dl, respectively. Her serum Ca(2+) and Pi were within the normal range (9.4 mg/dl and 5.4 mg/dl, respectively). Her intact parathyroid hormone (PTH) level was 1 730 000 pg/ml. A (99m)Tc-methoxy-isobutylisonitrile scintigraphy showed high uptake in three parathyroid glands. A magnetic resonance image showed microadenoma in the pituitary gland. The serum gastrin level was high. Genetic examination revealed a mutation of the MEN1 gene (894-9 G --> A). From these findings, she was diagnosed with multiple endocrine neoplasia (MEN) type 1. Subsequently, a parathyroidectomy was performed successfully, a parathyroid gland was transplanted to her right forearm, and her serum Ca(2+) level was controlled at 8.5-9.0 mg/dl. It is very important to identify MEN1 if an end-stage renal disease (ESRD) patient has hyperparathyroidism with multigland involvement. Examination of the MEN1 gene may be valuable to make an accurate diagnosis and choose the appropriate therapy in some ESRD patients with hyperparathyroidism.
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PMID:Multiple endocrine neoplasia type 1 in end-stage renal failure. 1561 41


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