Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine patients were studied 1.5--3 years after jejuno-ileostomy for obesity by an intravenous glucose infusion technique designed to imitate blood glucose concentrations after glucose ingestion. Whereas serum insulin and gastrin concentrations were normal, blood glucose concentrations were significantly depressed compared to preoperative levels as well as to levels in matched normal subjects. Thus, in the fasting state mean concentrations (+/- S.E.M.) of blood glucose, serum insulin and gastrin in the patients were, respectively, 3.3 +/- 0.2 mmol/l, 95 +/- 22 pmol/l and 38 +/- 4 pmol/l. The corresponding concentrations in the matched normals were 4.3 +/- 0.2 mmol/l, 70 +/- 18 pmol/l and 39 +/- 6 pmol/l. The glucose concentrations in the patients were low in all situations, i.e. in the fasting state, after oral glucose ingestion and during the intravenous glucose infusion. The results indicate that jejuno-ileostomy in obesity greatly facilitates peripheral glucose disposal. The mechanism behind this phenomenon is not yet known.
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PMID:Increased glucose disposal after jejuno-ileostomy. 76 35

In a retrospective study the basal and food-stimulated serum concentrations of gastrin and gastric secretion of acid were studied in 28 patients following three types of intestinal shunt operation for obesity. In each type 48 cm of functioning small intestine was preserved, but the ratio between functioning jejunum and ileum was different. The basal and stimulated concentrations of gastrin in serum were significantly higher in patients with the shortest jejunum in function. There was no difference in the gastric acid output. The study suggests that gastrin participates in evoking the gastric hypersecretion of acid which follows massive bowel resection or bypass. Deprivation of a hormonal inhibitory substance from the upper jejunum may be responsible for the increased serum gastrin concentration.
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PMID:Gastrin response to food after three types of intestinal shunt operations for obesity. 106 48

Jejunolieal bypass (JIB) patients provide a unique opportunity to study the relationship between small bowel loss and gastric secretory function. Preoperatively, and approximately one year postoperatively, measurements of gastric secretion were taken in 37 patients who underwent JIB for massive obesity. Basal acid output increased by 0.52 plus or minus 0.35 mEq/hr (P greater than.2), and peak stimulated acid output increased by 1.99 plus or minus 0.96 mEq/30 min (P smaller than .05). A separate group of 26 postoperative and 17 preoperative (control) JIB patients had fasting serum gastrin levels measured by radioimmunoassay. Postoperative patients had levels of 37 plus or minus 5 pg/ml, and control patients had levels of 36 plus or minus 4 pg/ml (P greater than .5). We conclude that following JIB for obesity, there is no significant change in basal acid secretion or in serum gastrin. There is a small, but statistically significant, increase in peak stimulated acid output. We currently find no clinical correlation with this change.
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PMID:Gastric secretion and serum gastrin in human small bowel bypass. 115 46

Gastric bypass as a 90 per cent gastric exclusion operation was used in 393 patients with massive obesity to limit food intake. Stomal ulcer has occurred in 1.8 per cent of such patients or one ulcer per 140 man years of observation. The studies of indwelling fundic pH and of gastric acid secretion from the excluded stomach indicate that acid secretion is reduced after gastric bypass but that the acid, unbuffered by food in the excluded stomach, results in a lowered gastrin secretion after a meal. Thus, gastric bypass in inhibitory to acid secretion in most morbidly obese patients who do not have known acid peptic disease.
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PMID:Effect of gastric bypass on gastric secretion. 125 57

Plasma concentrations of regulatory peptides were monitored in groups of obese and normal-weight subjects following modified sham feeding and a liquid fatty meal. Following modified sham feeding a significant increase in immunoreactive cholecystokinin (CCK) in plasma was recorded in both groups. In the obese subjects, however, the concentrations following sham feeding were significantly lower than in normal-weight subjects, and the initial part of the response was negative. Basal and modified sham feeding stimulated immunoreactive pancreatic polypeptide (PP) concentrations in plasma did not differ between the groups. After the liquid fatty meal plasma CCK concentrations increased similarly in both groups. In contrast immunoreactive neurotensin and somatostatin concentrations following the meal were lower in the obese group, and a changed concentration-time pattern for somatostatin was observed in the obese group. Postprandial concentrations of PP and immunoreactive gastrin were not different in the groups. The results indicate that the plasma concentration patterns of CCK, somatostatin and NT are disarranged in obesity. The changes may promote rapid propulsion and absorption of ingested food, and facilitate deposition of fat in adipose tissue in obesity and thus may be of pathophysiological importance.
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PMID:Plasma concentrations of regulatory peptides in obesity following modified sham feeding (MSF) and a liquid test meal. 134 61

The effects of oral diethylaminoethyl-dextran (3 g total), taken 30 min before a standard mixed test meal, on plasma glucose, total cholesterol, triglycerides, total lipids, gastrin-like immunoreactivity, bombesin-like immunoreactivity, gastric-inhibitory-polypeptide-like immunoreactivity and neurotensin-like immunoreactivity were evaluated in eight healthy volunteers following a double-blind protocol. Incremental peak plasma concentrations of total lipids and triglycerides were significantly reduced by pretreatment with diethylaminoethyl-dextran pretreatment, while peaks of plasma glucose and total cholesterol were not significantly affected. Diethylaminoethyl-dextran also inhibited postprandial gastrin-like gastric-inhibitory-polypeptide-like and neurotensin-like immunoreactivity; by contrast, bombesin-like immunoreactivity was not significantly modified. The present study indicates that diethylaminoethyl-dextran is able to regulate some postprandial metabolic and hormonal parameters in man; consequently it might be useful in the treatment of hyperlipoproteinaemia and obesity.
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PMID:Short-term effects of diethylaminoethyl-dextran on postprandial gastrointestinal hormone responses in man. 169 37

We recruited 10 patients with anorexia nervosa and 6 age- and height-matched control subjects. Basal and postprandial concentrations of glucose, insulin, cholesterol, amino acids, gastrin, and pancreatic polypeptide (PP) were measured in response to a standard mixed meal. The only satiety signal that was significantly different between the anorectic group and the control group was PP (P less than 0.001). Tryptophan-LNAA and tyrosine-LNAA ratios were not significantly different in the two groups; however, there was a trend toward a lower tryptophan-LNAA ratio in the anorectic group. Gastrin concentrations were significantly decreased in the anorectic group (P less than 0.001) as were basal insulin concentrations (P less than 0.05). Decreased gastrin concentrations may play a role in the gastric symptoms associated with anorexia nervosa. Previous findings that PP release is diminished in obesity, together with the present findings of PP increase in anorexia nervosa, suggest that this peptide may play a role in appetite control mechanisms.
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PMID:Potential regulators of feeding behavior in anorexia nervosa. 172 17

Impaired gallbladder emptying has been suggested as a possible factor in the pathogenesis of gallstones. Obese people have an increased incidence of gallstones, but there is no evidence of this in nonobese large people. This study was undertaken to determine if abnormal gallbladder motility is present in obese people. Fasting gallbladder volumes were determined using real-time ultrasound in 18 morbidly obese subjects whose weights were in a steady state [45 kg (100 lb) over ideal weight or twice expected weight for age and height; 9 males, 9 females], 18 age- and sex-matched volunteers of average size, and 18 nonobese large normal males (9 tall, 9 muscular). Gallbladder emptying studies with 99mtechnetium-diisopropyliminodiacetic acid were performed using 200 ml of 10% cream as a stimulus. The small-volume liquid fatty meal contained 113indium-diethylenetriaminepentaacetic acid to control for differences in gastric emptying in obesity. The gallbladder emptying rate in large people, both obese and nonobese, was less than that in normals of average size (p = 0.05). Fasting gallbladder volumes in large people were: obese, 41 ml (37-66 ml) (median; 95% confidence limits); nonobese large normal, 40 ml (27-43 ml). These values were greater than in normals of average size [17 ml (14-21 ml) (p = 0.03)]. Postprandial gallbladder volumes were also greater in large people: obese, 15 ml (8-23 ml); nonobese large normal, 20 ml (13-23 ml) compared with 2 ml (1-5 ml) in normals of average size (p less than 0.05). There were no differences between obese and nonobese large people. There were no differences in gastric emptying rates or in cholecystokinin, gastrin, motilin, and secretin release between obese and normal subjects. Gallbladder volume is crudely proportional to body size. Although fasting and postprandial volumes are greater in obesity, this is also present in nonobese, relatively size-matched controls. These data do not support a role for impaired gallbladder emptying in gallstone formation in obese patients whose weights are in a steady state.
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PMID:Increased volume and decreased emptying of the gallbladder in large (morbidly obese, tall normal, and muscular normal) people. 217 26

The concentrations and contents of immunoreactive substance P (SP), neurokinin A (NKA), vasoactive intestinal polypeptide (VIP) and gastrin releasing peptide (GRP) were measured in acid-ethanol extracts of intestine (duodenum-jejunum-ileum) and pancreas of C57BL/KsJ diabetes-obese (db/db) mice, Aston obese-hyperglycaemic (ob/ob) mice, and their respective lean controls. The intestinal concentration of GRP and pancreatic concentrations of VIP and GRP were 36-57% lower in lean Aston mice than lean C57BL/KsJ mice, indicating the influence of genetic background in control mice. Intestinal concentrations of SP and NKA were reduced by 19-33% in the db/db and ob/ob mutants compared with their lean controls, but the intestinal contents of these peptides were normal or greater than normal due to intestinal hypertrophy of the mutant mice. The intestinal VIP concentration was not altered, but the content was increased by 87% and 25% respectively in db/db and ob/ob mice, whereas the intestinal GRP concentration was reduced by 51% in ob/ob mice. Pancreatic concentrations and contents of NKA, VIP and GRP were similar in lean and db/db C57BL/KsJ mice. However, pancreatic concentrations and contents of VIP and GRP were reduced by 51-55% in ob/ob mice compared with their lean controls. The sensitivity of the present assay did not permit accurate determination of the low pancreatic concentrations of SP. The results suggest that the spontaneous ob/ob and db/db syndromes of obesity and diabetes in mice are associated with reduced intestinal concentrations of SP and NKA. The ob/ob mouse also exhibited reductions of intestinal GRP and pancreatic GRP and VIP concentrations. These changes in regulatory peptides may relate to abnormalities of intestinal and possibly pancreatic function in obese and diabetic mutant mice.
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PMID:Substance P, neurokinin A, vasoactive intestinal polypeptide and gastrin releasing peptide in the intestine and pancreas of spontaneously obese-diabetic mice. 243 55

In this study, gastrin release in the obese Zucker rat was investigated by in vivo and in vitro experiments. Obese rats exhibited normal plasma gastrin levels at 3 weeks (preobese), were moderately hypergastrinemic at 3 months and severely hypergastrinemic at 5 months, compared to lean littermates. Following oral peptone, plasma gastrin levels doubled in both lean and obese rats. Basal and vagally stimulated gastrin release from perfused stomachs was greater in obese compared to lean rats and atropine had no effect on basal gastrin release in either group. Basal somatostatin release from the perfused stomach was found not to differ in both groups of animals. Morphological studies revealed an increase in the number of gastrin-containing G-cells in adult obese rats compared to lean littermates, but not in 3-week-old pups compared to lean littermates, indicating a strong correlation between cell number and plasma gastrin levels. These data indicate that the obese Zucker rat exhibits fasting hypergastrinemia in vivo, a condition which appears after weaning and increases in severity with age. Gastrin hypersecretion persists from the vascularly perfused stomach preparation. The basal hypergastrinemia of the obese Zucker rat is independent of a hyperactive postganglionic cholinergic drive but is associated with and probably causally related to an increase in antral G-cell numbers.
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PMID:Gastrin release in obese Zucker rats. 256 9


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