gastrins and Weight-Gain

A group of 13 consecutive regularly menstruating women who gained at least 5 kg the previous year (Group I) was compared to a control group of similar age, parity, and social class (Group II). The two groups were similar in estimated and observed food intakes; pre- and postprandial gastrin levels; hourly 24-h profiles of cortisol and insulin; urinary cortisol and 17-hydroxycorticosteroids. Group I had higher serum prolactin concentrations at all times than Group II (mean values 14.60 micrograms/l vs. 8.84 micrograms/l; p = .0121). Galactorrhea was observed in 5 women from Group I and in none of the women from Group II (p < .05). Group I also differed from Group II in a higher incidence of meaningful life-events the year preceding the study, higher prevalence of sexual dysfunction (9/13 vs. 4/13; p < .01) and higher indexes (p < .05) of several parameters in the MMPI and SCL 90. Median serum cortisol and prolactin concentrations were negatively correlated, both in Group I (R = -.669; p = .012) and in the whole sample (R = -.453; p = .0298). It is suggested that the rapid weight gain is part of a neuroendocrine response to environmental stimuli also characterized by hyperprolactinemia. The significant negative correlation between serum prolactin and cortisol indicates that this response differs from, and is possibly an alternative to, the sympathoadrenal "stress" response.

Topics: Adult; Energy Intake; Feeding Behavior; Female; Gastrins; Hormones; Humans; Hydrocortisone; Insulin; Life Change Events; Obesity; Personality Assessment; Pituitary Neoplasms; Prolactin; Prolactinoma; Pseudopregnancy; Psychophysiologic Disorders; Reference Values; Stress, Psychological; Weight Gain

Priming of the gastrointestinal (GI) tract with low-volume feedings before giving full enteral feedings to very premature, high-risk infants is a controversial practice. We designed a study of infants weighing less than 1,250 g and receiving total parenteral nutrition to determine whether GI priming would hasten weight gain, improve tolerance of subsequent feedings, enhance nutritional status, and increase serum concentration of gastrin, a hormone trophic for intestinal growth. Infants were randomly assigned to receive total parenteral nutrition (TPN) alone (N = 21) or GI priming plus TPN (N = 19) for 12 days beginning on day 3 of life. Full-strength premature infant formula was used for priming. Both groups received the same total nutrition. Beginning on day 15, feedings in both groups were increased daily to a maximum of 120 kcal/kg/day on day 20, where they were maintained until day 30. After day 30, the feedings were modified according to the infants' condition. The groups did not differ in birth weight, gestational age, or 5-min Apgar scores. GI-primed infants had improved feeding tolerance after day 20 and a faster rise in serum gastrin during the initial phase of the study. There was no significant difference in weight gain. GI priming improves tolerance of feedings, accelerates rate of rise of serum gastrin during the first weeks of life, and does not increase the risk of feeding complications when compared to TPN alone. This may lead to more rapid maturation of the GI tract in primed infants.

Topics: Eating; Enterocolitis, Pseudomembranous; Female; Food Hypersensitivity; Gastrins; Humans; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature; Male; Parenteral Nutrition, Total; Prospective Studies; Random Allocation; Weight Gain

Enteroendocrine cells secrete over a dozen different hormones responsible for coordinating digestion, absorption, metabolism, and gut motility. Loss of enteroendocrine cells is a known cause of severe congenital diarrhea. Furthermore, enteroendocrine cells regulate glucose metabolism, with the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) playing critical roles in stimulating insulin release by pancreatic β-cells. Islet1 (Isl1) is a LIM-homeodomain transcription factor expressed specifically in an array of intestinal endocrine cells, including incretin-expressing cells. To examine the impact of intestinal Isl1 on glycemic control, we set out to explore the role of intestinal Isl1 in hormone cell specification and organismal physiology. Mice with intestinal epithelial-specific ablation of Isl1 were obtained by crossing Villin-Cre transgenic animals with mice harboring a Isl1(loxP) allele (Isl1(int) model). Gene ablation of Isl1 in the intestine results in loss of GLP-1, GIP, cholecystokinin (CCK), and somatostatin-expressing cells and an increase in 5-HT (serotonin)-producing cells, while the chromogranin A population was unchanged. This dramatic change in hormonal milieu results in animals with lipid malabsorption and females smaller than their littermate controls. Interestingly, when challenged with oral, not intraperitoneal glucose, the Isl-1 intestinal-deficient animals (Isl1(int)) display impaired glucose tolerance, indicating loss of the incretin effect. Thus the Isl1(int) model confirms that intestinal biology is essential for organism physiology in glycemic control and susceptibility to diabetes.

Topics: Age Factors; Animals; Animals, Newborn; Biomarkers; Blood Glucose; Cholecystokinin; Chromogranin A; Diarrhea; Dietary Fats; Enteroendocrine Cells; Female; Gastric Inhibitory Polypeptide; Gastrins; Genotype; Ghrelin; Glucagon-Like Peptide 1; Glucose Metabolism Disorders; Glucose Tolerance Test; Integrases; Intestinal Absorption; Intestinal Mucosa; Intestine, Small; LIM-Homeodomain Proteins; Malabsorption Syndromes; Male; Mice, Inbred C57BL; Mice, Knockout; Microfilament Proteins; Phenotype; Serotonin; Somatostatin; Transcription Factors; Weight Gain

Maternal obesity has been reported as a risk factor for various maternal and fetal complications. The aim of the present study was to examine the patterns of basal and postprandial plasma concentrations of certain gut hormones affecting food intake such as acylated ghrelin, peptide YY(3-36) (PYY(3-36)), cholecystokinin (CCK), insulin and glucose in pregnant women with varying body mass gain during physiological pregnancy. The study included 34 women with singleton pregnancies in the 2(nd) trimester of gestation. The examined pregnant women were divided into 4 groups; I. control pregnancy (CP) with weight gain below 0.5 kg/week; II. overweight low weight gain <1 kg/week (OLWG), III. overweight high weight gain >1 kg/week (OHWG); morbidly obese pregnant with weight gain >1.5 kg/week (MOP). The basal acylated-ghrelin levels in MOP subjects were significantly higher than those in CP and no usual suppression of acylated ghrelin after the meal observed in CP as well as in OLWG and OHWG was found in MOP women. Basal PYY(3-36) plasma levels were similar in CP, OLWG and OHWG but in MOP was significantly reduced and no significant increase in hormone level, typically observed in CP, was detected after a meal in overweight or obese women studied. The fasting CCK and C-reactive protein (CRP) levels in MOP subjects were significantly higher than those in CP and other overweight women. In conclusion, we found that pregnant women with overweight and obesity exhibit significant changes in fasting and postprandial gut hormones affecting food intake such as acylated ghrelin, PYY(3-36) and CCK as well as in CRP and these changes might contribute, at least in part, the development of obesity in pregnancy.

Topics: Acylation; Adult; Appetite; Blood Glucose; Body Mass Index; C-Reactive Protein; Cholecystokinin; Fasting; Female; Gastrins; Gastrointestinal Hormones; Ghrelin; Homeostasis; Humans; Insulin; Obesity; Obesity, Morbid; Peptide Hormones; Peptide YY; Poland; Postprandial Period; Pregnancy; Pregnancy Complications; Weight Gain

Heavy burdens of the abomasal nematode, Ostertagia (Telodorsagia) circumcincta, in growing lambs result in a reduction in liveweight gain due largely to a drop in voluntary feed intake. The present study investigated: (1) the role of subdiaphragmatic vagal and non-vagal visceral afferent nerves in mediating a reduction in voluntary feed intake, using subdiaphragmatic vagal deafferentation (vagotomy) either alone or in combination with coeliac-superior mesenteric ganglionectomy (vagotomy and sympathectomy); and (2) the association between appetite, abomasal pH, selected blood values (amidated gastrin (G-17-amide), glycine-extended gastrin (G-17-Gly), pepsinogen and leptin) and worm burden, in sheep experimentally infected with 100,000 O. circumcincta infective larvae per os. Neither vagotomy alone nor vagotomy and sympathectomy in combination adversely affected the establishment or course of development of the parasite burden, when compared with a control group subject to sham surgery. Furthermore, neither surgical procedure prevented the drop in appetite seen 5-10 days post-infection, although combined vagotomy and sympathectomy did reduce voluntary feed intake prior to the start of the study. Ostertagia infection resulted in a significant increase in abomasal pH in all three groups, which was accompanied by an increase in blood G-17-amide and in G-17-Gly, the latter reported for the first time in parasitized ruminants. There were no significant differences in blood leptin, also reported for the first time in parasitized sheep, either between groups or in comparison with pre-infection levels, though weak negative correlations were established between blood leptin and appetite from day 5 to the end of the study in all three groups and a positive correlation with blood G-17-amide in the control group over the same period. These data suggest that neither intact subdiaphragmatic vagal afferent nerves or coeliac-superior mesenteric ganglion fibres, nor changes in circulating gastrin and leptin concentrations play a major role in mediating the hypophagic effects of O. circumcincta in parasitized sheep.

Topics: Abomasum; Afferent Pathways; Animals; Anorexia; Energy Intake; Female; Gastrins; Hydrogen-Ion Concentration; Leptin; Male; Ostertagiasis; Random Allocation; Sheep; Sheep Diseases; Sympathectomy; Time Factors; Vagotomy; Weight Gain

The aim of the present study was to investigate the effects of repeated massage-like stroking on plasma levels of some gastrointestinal hormones, insulin included, glucose and weight gain. For this purpose, male rats were exposed to stroking on the ventral side of the abdomen for 3 or 14 times. The treatments were given every second day. Control rats were picked up at the same time but received no stroking. Body weight was measured regularly. Rats were decapitated 10 min after the last treatment. Hormone levels were radioimmunoassayed and glucose was measured by spectrophotometry. In rats exposed to 3 sessions of massage-like stroking plasma levels of insulin (p<0.05) and somatostatin (p<0.01) were significantly decreased 10 min after the last treatment. After 14 treatments of massage-like stroking, decreased plasma levels of insulin (p<0.01) and gastrin (p<0.01) as well as increased glucose levels (p<0.01) were observed 10 min after the last treatment. In addition, weight gain was significantly increased (ANOVA p<0.0001) in rats exposed to 14 treatments. In conclusion, repeated massage-like stroking decreased plasma levels of gastrin, insulin and somatostatin, increased plasma levels of glucose and promoted weight gain. The effects were influenced by the number of treatments.

Topics: Animals; Autonomic Nervous System; Blood Glucose; Gastrins; Insulin; Male; Massage; Neurosecretory Systems; Oxytocin; Rats; Rats, Sprague-Dawley; Somatostatin; Vagus Nerve; Weight Gain

Ghrelin, a 28-amino-acid peptide, has recently been isolated from the rat stomach as an endogenous ligand for the GH secretagogue receptor. We have reported previously that central or peripheral administration of ghrelin stimulates food intake, and the secretion of GH and gastric acid in rats. In the present study, we investigated how much endogenous centrally released ghrelin is involved in the control of food intake and body weight gain. We also examined the profile of ghrelin secretion from the stomach by RIA using two kinds of anti-ghrelin antiserum, one raised against the N-terminal ([Cys(12)]-ghrelin[1-11]) region and one raised against the C-terminal ([Cys(0)]-ghrelin [13-28]) region of the peptide. The former antibody recognizes specifically ghrelin with n- octanoylated Ser 3 (acyl ghrelin), and does not recognize des-acyl ghrelin. The latter also recognizes des-acyl ghrelin (i.e. total ghrelin). Intracerebroventricular treatment with the anti-ghrelin antiserum against the N-terminal region twice a day for 5 days decreased significantly both daily food intake and body weight. Des-acyl ghrelin levels were significantly higher in the gastric vein than in the trunk. Either fasting for 12 h, administration of gastrin or cholecystokinin resulted in increase of both acyl and des-acyl ghrelin levels. The ghrelin levels exhibited a diurnal pattern, with the bimodal peaks occurring before dark and light periods. These two peaks were consistent with maximum and minimum volumes of gastric content respectively. These results suggest that (1) endogenous centrally released ghrelin participates in the regulation of food intake and body weight, (2) acyl ghrelin is secreted from the stomach, (3) intestinal hormones stimulate ghrelin release from the stomach, and (4) regulation of the diurnal rhythm of ghrelin is complex, since ghrelin secretion is augmented under conditions of both gastric emptying and filling.

Topics: Animals; Cholecystokinin; Circadian Rhythm; Eating; Electric Stimulation; Fasting; Gastric Mucosa; Gastrins; Growth Hormone-Releasing Hormone; Immune Sera; Male; Radioimmunoassay; Rats; Rats, Wistar; Vagus Nerve; Weight Gain

Elemental diets cause intestinal atrophy and reduced intestinal integrity, which can lead to significant increases in intestinal permeability and bacterial translocation. Recently, several lectins have been shown to have trophic effects on the intestine.. We examined the effects of concanavalin-A and phytohaemagglutinin on cell proliferation and crypt fission throughout the intestine of mice fed on elemental diets.. Mice were randomized to chow fed, elemental diet, elemental diet plus concanavalin-A and elemental diet plus phytohaemagglutinin groups. Cell proliferation and crypt fission were estimated in microdissected crypts. Plasma gastrin and enteroglucagon levels were measured by radioimmunoassay.. Elemental diet feeding significantly decreased cell proliferation and crypt fission of the middle and distal small intestine and throughout the colon. Phytohaemagglutinin significantly increased the weight of the intestine, but concanavalin-A had little effect. Cell proliferation in the small intestine was significantly increased by both lectins. However, in the stomach and colon, only phytohaemagglutinin increased proliferation. Crypt fission in the colon was dramatically increased by phytohaemagglutinin. Phytohaemagglutinin increased the plasma gastrin level, but not the enteroglucagon level.. Lectins have significant trophic effects on the small intestine and colon of mice fed elemental diets, and these actions vary between different sites in the gastrointestinal tract.

Topics: Animals; Atrophy; Cell Division; Colon; Concanavalin A; Food, Formulated; Gastric Mucosa; Gastrins; Intestine, Small; Lectins; Male; Metaphase; Mice; Organ Size; Phaseolus; Phytohemagglutinins; Plant Lectins; Radioimmunoassay; Random Allocation; Stomach; Weight Gain

The stomach is rich in endocrine cells, including those producing ghrelin, which is thought to play a role in the control of body growth. Omeprazole treatment is associated with hypergastrinaemia, resulting in growth of the oxyntic mucosa in general and the enterochromaffin-like (ECL) cells in particular. In the present study, we examined the effects of long-term omeprazole treatment on young male rats with respect to body growth and stomach.. Male rats (24 days old) were treated with omeprazole (400 micromol/kg/day) or vehicle for 77 days. The body weight was recorded twice per week. At sacrifice, dual-energy X-ray absorptiometry (DXA) was used to assess total bone area, bone mineral content (BMC), bone mineral density (BMD) and body composition (fat and lean body mass). The lengths of the spine and the femur were recorded. The plasma concentrations of gastrin and histamine were determined by radioimmunoassays. The endocrine cells of the stomach were examined by immunocytochemistry.. The body weight gain was suppressed by omeprazole treatment. The bone area, BMC and BMD were reduced, while the lengths of the spine and the femur and the body composition were unchanged. Omeprazole-induced hypergastrinaemia was associated with enlargement of the oxyntic area and with hyperplasia of ECL cells but not of A-like cells and D cells. In contrast, the enterchromaffin (EC) cell density in the antrum was reduced.. Omeprazole treatment of young male rats reduces body weight and bone mass gain. The densities of ECL cells in the oxyntic mucosa was increased and of the EC cells in the antral mucosa reduced.

Topics: Age Factors; Animals; Anti-Ulcer Agents; Bone Diseases, Metabolic; Calcification, Physiologic; Enterochromaffin-like Cells; Enzyme Inhibitors; Gastrins; Ghrelin; Male; Omeprazole; Peptide Hormones; Peptides; Rats; Rats, Sprague-Dawley; Stomach; Weight Gain

Histamine-forming ECL cells in the rat stomach operate under the control of gastrin. They represent a convenient target for studying cholecystokinin-B/gastrin (CCK(2)) receptor antagonists in vivo. We examined the effectiveness and duration of action of two CCK(2) antagonists, YM022 and YF476, with respect to their effect on ECL-cell histidine decarboxylase (HDC) activity in the rat. Oral administration of subcutaneous deposition of YF476 or YM022 reduced the HDC activity. The maximum/near-maximum dose for both drugs and for both modes of administration was 300 micromol kg(-1) (effects measured 24 h after dose). At this dose and time the serum concentration of YF476 was 20 - 40 nmol l(-1). The dose 300 micromol kg(-1) was used in all subsequent studies. A single subcutaneous injection of YF476 inhibited the HDC activity for 8 weeks. The circulating concentration of YF476 remained high for the same period of time (>/=15 nmol l(-1)). Subcutaneous YM022 suppressed the HDC activity for 4 weeks. A single oral dose of YF476 or YM022 inhibited the HDC activity for 2 - 3 days. Chronic gastric fistula rats were used to study the effect of subcutaneous YF476 on gastrin-stimulated acid secretion. A single injection of YF476 prevented gastrin from causing an acid response for at least 4 weeks (the longest time studied). We conclude that a single subcutaneous injection of 300 micromol kg(-1) YF476 causes blockade of CCK(2) receptors in the stomach of the rat for 8 weeks thus providing a convenient method for studies of the consequences of long-term CCK(2) receptor inhibition.

Topics: Administration, Oral; Animals; Benzodiazepines; Benzodiazepinones; Dose-Response Relationship, Drug; Gastric Acid; Gastric Mucosa; Gastrins; Histidine Decarboxylase; Hormone Antagonists; Injections, Subcutaneous; Male; Phenylurea Compounds; Rats; Rats, Sprague-Dawley; Receptor, Cholecystokinin B; Receptors, Cholecystokinin; Weight Gain

Parenterally nourished preterm infants commonly receive minimal enteral feedings, the aim being to enhance intestinal function. Whether this regimen increases intestinal growth has not been established.. Our objective was to determine the minimal enteral nutrient intakes necessary to stimulate and to normalize neonatal intestinal growth.. Intestinal growth and cell proliferation were quantified in neonatal pigs given equal amounts of an elemental nutrient solution for 7 d. Different groups (n = 5-7 per group) received 0%, 10%, 20%, 40%, 60%, 80%, or 100% of total nutrient intake enterally, with the remainder given parenterally.. In the jejunum, wet weight, protein mass, and villus height were significantly greater at enteral intakes >40%. Stimulation of ileal protein mass required a higher enteral intake (60%). In both segments, abrupt increases in DNA mass, crypt depth, ornithine decarboxylase activity, and crypt cells in S-phase occurred between enteral intakes of 40% and 60%. Circulating concentrations of glucagon-like peptide-2 and peptide YY, but not gastrin, increased significantly between enteral intakes of 40% and 60% and closely paralleled indexes of cell proliferation.. The minimal enteral nutrient intake necessary to increase mucosal mass was 40% of total nutrient intake, whereas 60% enteral nutrition was necessary to sustain normal mucosal proliferation and growth. Our results imply that providing <40% of the total nutrient intake enterally does not have significant intestinal trophic effects.

Topics: Animals; Animals, Newborn; Cell Division; DNA; Enteral Nutrition; Food, Formulated; Gastrins; Glucagon-Like Peptide 2; Glucagon-Like Peptides; Ileum; Intestines; Jejunum; Nutritional Requirements; Organ Size; Peptide YY; Peptides; Proteins; Swine; Weight Gain

Gastrectomy leads to osteopenia in the rat. The present study describes the effects of gastrectomy on bone morphology. Rats were subjected to gastrectomy or sham operation. Four weeks after the operation the rats were killed and both tibiae were removed. Bone morphology of the left tibia was analyzed with quantitative computer tomography, the right tibia with histomorphometry. Bone length, bone mineral content, as well as indices of bone resorption and formation were measured in the metaphysis and the diaphysis. Gastrectomy had no effect on longitudinal bone growth but it led to a low bone mineral content at both sites. Bone resorption was increased by gastrectomy, as shown by an increase in the medullary cavity area in the diaphysis. Gastrectomy also reduced bone formation, as shown by a decreased periosteal circumference and a decrease in the mean periosteal bone apposition in the diaphysis. In conclusion, gastrectomy-evoked osteopenia reflects impaired formation and increased resorption of bone.

Topics: Animals; Body Weight; Bone and Bones; Bone Density; Bone Diseases, Metabolic; Bone Regeneration; Bone Resorption; Calcification, Physiologic; Calcitonin; Calcium; Diaphyses; Gastrectomy; Gastrins; Male; Osteogenesis; Parathyroid Hormone; Periosteum; Rats; Rats, Sprague-Dawley; Tibia; Weight Gain

Chronic infection with Helicobacter pylori causes persistent elevations in gastric juice ammonia levels. Thus, we studied the effects of experimentally induced increases in gastric juice ammonia levels on gastric structure and function and gastrin homeostasis.. Rats were fed either normal chow or the diet supplemented (20 g/dL) with ammonium or sodium acetate.. Long-term dietary ammonium loading for 2 weeks or longer resulted in a 1.5-2-fold increase in the weight and mucosal thickness of the stomach and proximal duodenum with evidence of mild gastritis and enterochromaffinlike cell hyperplasia. The ammonium-containing diet also induced a significant 2-3-fold increase in both circulating gastrin levels of fed rats and an increase in the postprandial gastrin responses over control values. Antral gastrin levels were also markedly elevated by long-term ingestion of the test diet, which was increased 3-4-fold over control values in fasted animals and less so after meal stimulation. Consistent with these findings, gastrin-specific messenger RNA was increased 2.5-3-fold in the antrum of ammonium fed rats, whereas actin-specific messenger RNA was not affected or decreased. Animals fed a diet supplemented with 20 g/dL sodium acetate sustained modest increases in mucosal thickness and serum and antral gastrin concentration, suggesting that nonspecific gastric injury and inflammation is also a factor that influences G-cell function.. Long-term exposure of the antral mucosa to elevated levels of ammonia in the gastric juice in the presence of gastritis, conditions similar to that occurring in subjects infected with H. pylori, seem to be causative factors in the development of G-cell hyperfunction.

Topics: Acetates; Ammonia; Animals; Duodenum; Gastric Mucosa; Gastrins; Hydrogen-Ion Concentration; Intestinal Mucosa; Male; Pyloric Antrum; Rats; Rats, Sprague-Dawley; Stomach; Weight Gain

Omeprazole, a long-acting inhibitor of gastric acid secretion, is able to increase the circulating concentrations of gastrin. Daily treatment with high doses of omeprazole cause sustained hypergastrinemia. Long-standing hypergastrinemia can be expected to exert numerous effects in the body. For instance, gastrin has been proposed to promote growth in the digestive tract and pancreas. The present study is concerned with the effect of omeprazole on parathyroid glands in the chicken.. Chickens were treated with omeprazole (400 mumol/kg/day) in methylcellulose (2.5 ml/kg) for 5 or 10 weeks. Controls received vehicle. Blood calcium and serum gastrin concentrations were studied. The weight gain of the animals and of various organs (proventriculus, antrum, thyroids, parathyroids, ultimobranchial glands, and femur) were determined. The DNA content and the size of the parathyroid chief cells were also determined.. Omeprazole reduced the body weight gain while greatly increasing the weight of the proventriculus and the parathyroid glands. The weight and density of the femur were reduced. The circulating concentrations of calcium were unaffected. The DNA content of the parathyroid glands was increased, and morphometric analysis of the parathyroid chief cells showed an increased cell size. Thus, the increased parathyroid gland weight seems to reflect both hypertrophy and hyperplasia. There was a slight increase in the weight of the ultimobranchial glands (expressed per kilogram body weight). The weight of the thyroids was unaffected (expressed in relation to body weight).. The results indicate that omeprazole treatment in chickens leads not only to trophic effects in the acid-producing gastric mucosa (probably because of the ensuing hypergastrinemia), as reported earlier, but also to growth of the parathyroid glands (both hypertrophy and hyperplasia) and to bone loss without affecting blood calcium values. The mechanism behind these effects remains unknown.

Topics: Animals; Bone Density; Chickens; DNA; Gastrins; Hyperplasia; Hypertrophy; Omeprazole; Organ Size; Parathyroid Glands; Proventriculus; Thyroid Gland; Weight Gain

Effects of strategic anthelmintic treatment on pathophysiologic and immunomologic changes induced by infection with Ostertagia ostertagi and Cooperia oncophora were studied in 2 groups, of 12 calves each: an infected group, inoculated with 200,000 mixed O ostertagi and C oncophora third-stage larvae (L3) on day 1; and an infected-treated group, similarly inoculated, but treated with ivermectin at 9 and 33 days. All calves were also inoculated at 12 weeks with Brucella abortus vaccine, at 13 weeks with bovine rhinotracheitis vaccine (bovine herpesvirus 1), and at 14 weeks with a soluble O ostertagi L3 extract, then were allowed to graze on a contaminated pasture. Four calves from each group were slaughtered at 7, 11, and 19 weeks of the study. Calves of the infected group had significantly (P < 0.05) lower weight gain than did those in the infected-treated group (60.90 kg vs 75.86 kg). They also had high plasma pepsinogen and serum gastrin values, and low serum albumin concentration from 2 or 4 weeks. Calves in the infected-treated group had steady weight gain and no significant changes in albumin and gastrin values. They also had less severe abomasal lesions and higher carcass yield. Compared with calves of the infected-treated group, those of the infected group had significantly (P < 0.05) lower blood lymphocyte reactivity to phytohemagglutinin at 14 and 16 weeks, to concanavalin A at 10 weeks, to pokeweed mitogen at 14 weeks, and to soluble O ostertagi L3 extract at 2, 4, and 14 weeks. (ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Anthelmintics; Body Weight; Brucella abortus; Brucella Vaccine; Cattle; Cattle Diseases; Gastrins; Gastrointestinal Diseases; Herpesvirus 1, Bovine; Lymphocyte Activation; Lymphocytes; Male; Nematoda; Nematode Infections; Orchiectomy; Ostertagiasis; Parasite Egg Count; Pepsinogens; Time Factors; Viral Vaccines; Weight Gain

Pathophysiologic effects of Ostertagia ostertagi infection and their prevention by strategic anthelmintic treatments were studied in 3 groups each of 6 steer calves. Group-1 calves were noninfected controls. Group-2 calves were inoculated with 100,000 third-stage larvae on the 1st and 28th days of the experiment and grazed on pasture initially free of contamination. Group-3 calves were on a similar regimen as those in group 2, but were also treated with ivermectin 9 days after each larval inoculation. Group-2 calves had increased plasma pepsinogen and gastrin values and decreased weight gains, and total serum protein and albumin concentrations from the 2nd week of infection onward. They were anemic at 10 to 12 weeks and had lower carcass and meat quality at slaughter. Strategic anthelmintic treatments were effective in preventing these effects and calves in groups 1 and 3 had similar performances. On the basis of our findings, high pepsinogen values were related to worm burdens, whereas high gastrin concentrations were related to gastric lesions.

Topics: Abomasum; Animals; Blood Proteins; Blood Urea Nitrogen; Cattle; Cattle Diseases; Feces; Gastrins; Hematocrit; Ivermectin; Male; Meat; Nutritional Status; Ostertagia; Ostertagiasis; Parasite Egg Count; Pepsinogens; Random Allocation; Serum Albumin, Bovine; Weight Gain

We studied the effects of dietary calcium, fat and fiber on serum gastrin in Fischer-344 rats in a full factorial experiment as part of a larger study of diet and colon cancer risk factors. Nine- to 10-wk-old male rats were fed standard or experimental diets for 4 wk. Wheat bran was the sole source of fiber. Wheat bran levels were 0, 2.5, 10 and 20%; fat levels were 1, 5 and 10%; calcium levels were 0.18, 0.52 and 1.04% of diet weight. On d 29 serum was collected and stored at -80 degrees C until analyzed. There was a significant (P less than 0.0001) dose-dependent increase in serum gastrin from 102 to 173 ng/L, with increasing calcium. No other significant changes in serum gastrin were noted with the dietary changes. A long-term change in the level of serum gastrin, caused by dietary modification, will influence the trophic effect that gastrin has on colonic mucosa as well as on colon carcinomas. We speculate that calcium supplementation, although slowing colonic proliferation, might have an undesirable effect on the growth of early undetected colonic tumors.

Topics: Adenocarcinoma; Animals; Calcium, Dietary; Colonic Neoplasms; Dietary Fats; Dietary Fiber; Gastrins; Male; Rats; Rats, Inbred F344; Risk Factors; Triticum; Weight Gain

This study was conducted to evaluate the effects of tactical treatments with ivermectin against trichostrongyles in first-season grazing heifer calves in the Danish marshland. A group of Black-Pied Friesian calves was turned out in early May on a permanent pasture naturally infected with trichostrongyle larvae. In late July, when high herbage infectivity started to appear, the pasture was divided into two plots of equal size, which from then and until housing in late October were each grazed by half of the original group of calves. One of these groups was given three anthelmintic treatments with ivermectin at 4-week intervals starting in late July. The other group served as non-treated controls. Ostertagia ostertagi and Cooperia oncophora were the predominant trichostrongyles. Nematodirus helvetianus was observed on few occasions. Although the animals were exposed to a high herbage infectivity from July onwards, the anthelmintic treatments conferred a significant reduction in trichostrongyle loads, as evidenced by an almost complete cessation of egg excretion and a significant lowering of pepsinogen and gastrin levels in the blood. This was reflected in higher weight gains.

Topics: Animals; Cattle; Cattle Diseases; Feces; Female; Gastrins; Intestinal Diseases, Parasitic; Ivermectin; Ostertagia; Ostertagiasis; Parasite Egg Count; Pepsinogens; Seasons; Serum Albumin, Bovine; Trichostrongyloidea; Trichostrongyloidiasis; Weight Gain

Two outbreaks of parasitic gastroenteritis were observed in a group of 10 first-season grazing calves, one in mid-July and one in mid-September. In both cases emergency anthelmintic treatment was needed to prevent further damage. Severe clinical signs were observed together with high faecal egg counts and high serum pepsinogen and gastrin concentrations. Low total protein and albumin concentrations were also observed, especially during the second outbreak. The ostertagia antibody levels followed a similar pattern to the serum pepsinogen and gastrin concentrations. At the end of the housing period a mild type II ostertagiasis was observed. In the second grazing season the heifers did not show any signs of parasitic gastroenteritis, but there was a serious outbreak of husk which required treatment.

Topics: Animals; Antibodies, Helminth; Bronchitis; Cattle; Cattle Diseases; Disease Outbreaks; Gastrins; Gastroenteritis; Ostertagia; Parasite Egg Count; Pepsinogens; Seasons; Time Factors; Weight Gain

Topics: Amniotic Fluid; Cholecystokinin; Digestion; Digestive System Physiological Phenomena; Eating; Embryonic and Fetal Development; Endocrine Glands; Energy Metabolism; Female; Gastrins; Gastrointestinal Hormones; Growth; Humans; Infant; Infant, Newborn; Lactation; Pregnancy; Somatostatin; Sucking Behavior; Vagus Nerve; Weight Gain