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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to evaluate the effectiveness of a gastric implant in an animal model of dietary obesity, silicone implants (2.5 ml) were inserted into the stomachs of male rats maintained on a chow or "cafeteria" diet. At the time of implantation, the cafeteria fed rats weighed 14% more than chow fed controls. Overweight cafeteria fed animals lost weight in response to the gastric implant, whereas control chow fed animals did not. Both implant groups had significant increases in stomach weights in contrast to sham implant groups, but the increase was much less in the cafeteria diet group. The fasting plasma levels of the gastrointestinal hormones, gastrin and pancreatic polypeptide, and oxytocin (a marker of vagal afferent function) were measured by radioimmunoassay. Cafeteria fed sham or implanted animals had significantly higher fasting levels of plasma oxytocin and gastrin, and significantly lower plasma levels of pancreatic polypeptide than the chow fed groups. These studies demonstrate that the gastric implant has more effect on weight in overweight animals on a palatable mixed diet, perhaps related to both mechanical and neural factors.
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PMID:Effects of a gastric implant on body weight and gastrointestinal hormones in cafeteria diet obese rats. 275 19

The release of somatostatin from the pancreas and stomach following the ingestion of a meal and its increase in the peripheral circulation elicits an attenuation of postprandial hormone secretion such as insulin, pancreatic polypeptide and gastrin and retards the rate at which nutrients enter the circulation. Reduced tissue somatostatin content and/or an attenuated somatostatin release is associated with hyperinsulinism and obesity in certain animal models. In the obese Zucker rat, however, tissue somatostatin levels are increased and therefore the present study was designed to determine the effect of synthetic somatostatin on basal and postprandial arterial insulin levels in obese and lean Zucker rats. Synthetic somatostatin was infused at doses of 0.25, 0.5, 1 and 5 ng/kg X min before and after the intragastric instillation of a liver extract/sucrose test meal. In the obese rats somatostatin at a dose of 5 ng/kg X min reduced basal plasma insulin levels significantly, whereas no effect of somatostatin was observed on basal insulin levels in the lean animals at all doses employed. The integrated postprandial insulin response was reduced during 0.25, 0.5, 1 and 5 ng/kg X min somatostatin in the obese animals, whereas only 0.5 ng/kg X min and higher doses had an inhibitory effect in the lean rats. The degree of inhibition in relation to the postprandial insulin response during saline infusions was 35-230% in the obese and 30-100% in the lean Zucker rats within the range of somatostatin infusions employed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased sensitivity to somatostatin in obese Zucker rats. 285 37

This paper presents the first case of extensive, diffuse, somatostatin-immunoreactive D-cell hyperplasia in the human stomach and duodenum. It occurred in a 37-yr-old woman, who showed clinical signs of dwarfism, obesity, dryness of the mouth, and goiter. The density of the distribution of D cells was increased 39-fold in the stomach fundus, 23-fold in the proximal antrum, 25-fold in the distal antrum, and 31-fold in the upper duodenum in comparison with normal values. At the same time, the gastrin-immunoreactive cells were increased 2.3-fold in the antrum. Although the range in size of the D cells was within normal limits in all regions examined, the G cells showed pronounced hypertrophy of up to 127%. A possible relationship between the immuno-histochemical findings and the clinical picture is discussed.
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PMID:Diffuse somatostatin-immunoreactive D-cell hyperplasia in the stomach and duodenum. 287 99

Certain features of the body hormonal system participation in the realizing of the specific dynamic action of food (SDAF) were studied in 26 patients with exogenous constitutional obesity. The radioimmunoassay was used to estimate the levels of a number of hormones (gastrin, insulin, glucagon, triiodothyronine, thyrotrophin, adrenocorticotrophin and hydrocortisone) in the peripheral blood of the patients on an empty stomach (the basal level) and 1,2 and 4 hours after food protein intake. The control group consisted of 20 normal subjects. It has been shown that SDAF is a complex process of changing from the state of hunger to satiation that involves many regulatory components, both nervous and humoral. The study of the features of the SDAF development in health and disease presents valuable information on the mechanisms of metabolic disorders in the body in varying pathologic states including obesity.
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PMID:[Specific dynamic action of food in obese patients]. 303 2

The paper is concerned with the results of investigation of 26 donors and 85 patients with diabetes mellitus, type II, with normal body mass and obesity during GTT and a test breakfast to reveal correlation of IRI and IRG levels with the level of gastrin. Comparative analysis of indices during OGTT and food intake has shown that an increase in the levels of gastrin in patients with diabetes mellitus, type II, does not correlate with body mass and the total level of insulin, but it may correlate with a metabolically active form of insulin. During food intake the levels of gastrin rise and do not change during GTT. A rise of the level of gastrin in patients with diabetes mellitus, type II, during a test breakfast is accompanied by change in the level of insulin, its peak being lower than that during GTT. Attention was focused on a group of patients with a history of obesity in whom by the time of investigation body mass returned to normal and the level of glucose was decreased. However, gastrin and insulin levels were still high, and metabolic regulation was disturbed. Therefore, body mass normalization did not eliminate causative and pathogenetic factors of diabetes mellitus.
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PMID:[The role of gastrin in regulating insulin and glucagon secretion in patients with diabetes mellitus]. 305 84

We previously found that massively obese patients respond with less gastric acid secretion in response to vagal stimulation. This is compatible with the described association between experimental obesity and altered vagal function in the rat. To confirm this observation, the pancreatic and biliary responses to vagal stimulation were examined in nine nondiabetic obese patients against a background secretin infusion of 15 CU x h-1, and monitored after a subsequent injection of 75 IDU of cholecystokinin. Two separate marker perfusion systems were used in the stomach and duodenum, respectively, and blood samples were drawn for hormone analyses. In contrast to controls having normal body weight, the obese patients failed to respond with increments of pancreatic enzyme secretion and duodenal bile acids after stimulation with modified sham feeding. Cholecystokinin stimulated the pancreatic secretion of trypsin, amylase, and lipase, the emptying of bile acids, and the release of gastrin, but the patients' responses were only half that of the controls. In the resting state the obese had higher outputs of bile and pancreatic enzymes and higher plasma levels of pancreatic polypeptide compared with controls, but the pancreatic bicarbonate secretion rate was not different. The almost complete suppression of the basal gastric acid secretion by a low dose of intravenous (IV) secretin in controls did not occur in the obese. We conclude that massive obesity is associated with a reduced pancreatic and biliary response to vagal stimulation. Compared with controls, the digestive functions of the obese patients seem to be less sensitive to stimulation by exogenous cholecystokinin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired pancreatico-biliary response to vagal stimulation and to cholecystokinin in human obesity. 328 31

Studies in animals and man suggest involvement of the vagal nerve in the pathophysiology of massive obesity. An abnormal vagal response pattern has been found in the obese rat, but corresponding functional studies in obese man are nonexistent. The gastric acid secretion was therefore examined in 13 nondiabetic grossly obese patients (average body weight 120 kg) and compared to 16 age-matched controls of normal body weight. The gastric acid response to modified sham feeding was significantly (P less than 0.05) reduced in obese patients, being on average 60% of the control output. The obese patients had a higher maximal gastric acid response to graded intravenous pentagastrin, 36.6 +/- 2.9 mmol/hr, compared to 27.1 +/- 2.4 mmol/hr in controls (P less than 0.05). In addition, the patients seemed to need less pentagastrin to reach a secretory plateau. Basal acid secretion rates were similar in obese and control groups. Plasma gastrin and blood glucose were not significantly different in obese patients and controls, but patients had significantly elevated plasma insulin levels. The change of plasma insulin during the sham-feeding procedure correlated with the magnitude of the secretory response in obese and control subjects. The reduced gastric acid response to vagal stimulation in the absence of impaired parietal cell function in obese patients is indicative of an association between massive obesity and altered vagal function in man.
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PMID:Gastric secretion in massive obesity. Evidence for abnormal response to vagal stimulation. 330 91

The gastric acid secretion was studied in 17 extremely obese patients after injection of synthetic gastrin (Peptavlon). The mean basal acid output (BAO) and the peak acid output (PAO) were both within normal range. Positive correlation was found between PAO and body weight. Gastric banding was performed as treatment of the obesity, and the gastric acid secretion was studied in the proximal and the distal pouch after a mean postoperative interval of 8 (range 4-20) weeks. BAO was similar after banding, but PAO was significantly decreased (from 26.3 +/- 3.6 to 16.2 +/- 2.2 mmol/h). PAO and BAO were almost identical in the two pouches, despite great difference in their size.
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PMID:Gastric acid secretion in extremely obese subjects before and after gastric banding. 361 62

We determined gastrin and pepsinogen I in serum samples obtained in 1968-69 from 256 women (175 women 54 years old and 81 women 60 years old when sampled). The concentration of gastrin in serum was significantly (p less than 0.01) and positively correlated with the incidence of myocardial infarction during a 12-year follow-up, with age taken into account as a background variable in multivariate analysis. It was not correlated with overall mortality or with the 12-year incidences of angina pectoris, electrocardiographic changes indicating ischemic heart disease, or stroke. The correlation with myocardial infarction was independent of smoking, systolic blood pressure, indices of obesity, concentrations of blood glucose during fasting and of serum triglycerides and cholesterol, and of the presence of diabetes mellitus at screening or during follow-up. Serum gastrin was significantly (p less than 0.05) related to body mass index (positive age-specific relation) and to smoking (negative age-specific relation). These findings may provide a new aspect to analysis of risk factors for myocardial infarction.
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PMID:Hypergastrinemia--a risk factor for myocardial infarction? 397 91

There is evidence for involvement of gastrointestinal hormones in pathogenesis of obesity and reports on lipolytic activity in animals. The in vitro lipolytic activity of these hormones was tested in human adipocytes. Vasoactive intestinal polypeptide, glucagon, secretin, human gastrin I, gastrin releasing polypeptide, gastric inhibitory polypeptide, pancreatic polypeptide, motilin, bombesin, neurotensin, C-peptide, as well as cholecystokinin did not stimulate lipolysis significantly above basal. These results indicate that the involvement of these hormones in obesity in man might not be due to a direct lipolytic effect on the human adipocyte.
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PMID:Glycerol release from incubated human adipocytes is not affected by gastrointestinal peptides. 401 16


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