[Cecostomy in acute obstructive carcinoma of the left hemicolon].
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Biomedical subjects
Publications and source records attributed to K B Lauritsen.
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The aim of the study was to elucidate the differential role of the jejunum and ileum in the regulation of secretion of the gut hormones, gastrin, gastric inhibitory polypeptide, and enteroglucagon, and the pancreatic hormones, insulin, glucagon, and pancreatic polypeptide, in man. We measured the plasma levels of the hormones (and glucose) during fasting and after a test meal in 34 obese patients, of whom 5 were waiting for bypass surgery and 29 had had a jejunoileal bypass with a 3:1 or 1:3 jejunoileal ratio between the functioning segments 3, 9, or 15 months earlier. The major findings were that surgery bypass (1) has no important influence on the levels of gastrin and pancreatic polypeptide, (2) reduces the level of gastric inhibitory polypeptide, insulin (and glucose), and enhances the pancreatic glucagon level, independently of the jejunoileal ratio, and (3) increases enteroglucagon secretion, most effectively so with a short jejunal and long ileal segment left in continuity. These findings suggest that the upper jejunum and terminal ileum has no important role in regulation of secretion of these hormones apart from that in secretion in enteroglucagon which is related to the length of functioning ileum.
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The responses of gastric inhibitory polypeptide (GIP) and insulin to intraduodenal and IV triglyceride infusions were measured in 11 late fetal and 10 neonatal pigs. Basal plasma glucose, insulin, and GIP concentrations were lower in fetal than in neonatal pigs. In the fetal pigs, plasma glucose increased slightly during intraduodenal and IV triglyceride infusions, whereas plasma insulin remained unchanged during the tests. No significant changes were observed in plasma GIP concentration following intraduodenal triglyceride infusion in the fetal pigs, but plasma GIP fell during the IV infusion of triglyceride in these pigs (p less than 0.01). In the neonatal pigs, plasma glucose and insulin remained unaffected by intraduodenal and triglyceride infusions. Plasma GIP did not change during the IV triglyceride infusion, but exhibited a paradoxical decline after the intraduodenal triglyceride infusion (p less than 0.05). It is concluded that the GIP-cell response to an oral triglyceride load is suppressed in late fetal and neonatal pigs. The abolished GIP response to oral triglycerides could play a causal role in the inactivity of the enteroinsular axis which is seen in both human and animal neonates.
Eight patients with advanced renal failure of long duration were studied 1 day after hemodialysis. A 50 g oral glucose load (OGTT) and an intravenous glucose infusion (IVGI), giving the same plasma glucose profile as the OGTT, were carried our in order to study the relation between Gastric Inhibitory Polypeptide (GIP) plasma levels after oral glucose and the insulin release during OGTT and IVGI. The plasma GIP increase during OGTT was significantly elevated compared to a group of eight healthy volunteers. The insulin potentiation during OGTT in relation to GIP was significantly depressed in the uremic patients. It is proposed that a factor of intestinal origin is released during intake of carbohydrates, which blocks the B-cell response to the combined glucose-GIP stimulus. Alternatively, the concentrations of plasma GIp measured have included GIp fragments without insulin releasing capability.
The gastro-entero-pancreatic (GEP) hormone response to glucose ingestion is considerably altered in pregnancy in normal women and gestational diabetics. In normal women, also the GEP hormone response to protein is changed in pregnancy. In the present investigation, the gastrin, gastric inhibitory polypeptide (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, pancreatic glucagon, and pancreatic polypeptide (PP) responses to a protein rich meal in pregnancy and postpartum were studied in 10 women with gestational diabetes. Five of the women were overweight and five were normal weight. Fasting and postprandial gut GLI and PP levels were reduced and insulin levels enhanced in pregnancy. No effect of pregnancy on fasting or postprandial gastrin, GIP, or glucagon levels was found. In pregnancy as well as postpartum, insulin levels were higher in the overweight than in the normal weight patients, whereas the concentrations of the other hormones were similar in the two subgroups of gestational diabetics. It is concluded that the GEP hormone response to a protein rich meal is influenced by late pregnancy in gestational diabetics in the same way as in normal women. The physiological consequences of the findings are not known in detail as yet but they may be important to carbohydrate metabolism and gastrointestinal physiology in pregnancy.
Eight patients with biopsy-verified coeliac disease were investigated after remission on a gluten-free diet. A 50-g oral glucose load (OGTT) and an intravenous glucose infusion (IVGI) giving the same plasma glucose profile as the OGTT were carried out. The relation between gastric inhibitory polypeptide (GIP) plasma levels after oral glucose and the insulin release during OGTT and IVGI were studied. Plasma GIP concentration in the fasting state and the increase in plasma GIP during OGTT were significantly lower than in a group of eight healthy volunteers. However, the insulin potentiation during OGTT, the incretin effect, was normal. The results indicate the existence of other incretins than GIP. These are probably released from the distal small bowel in patients with coeliac disease.
Six duodenal ulcer patients were investigated before and 3 months after truncal vagotomy and pyloroplasty. Plasma concentrations of gastric inhibitory polypeptide (GIP), insulin, and glucose were measured during intrajejunal infusion of 50 g of glucose. The GIP response was significantly diminished postoperatively; insulin and glucose concentrations, however, were unchanged. The reduction of GIP release was positively correlated with the reduction of the peak acid output. The results suggest that a reduced vagal innervation of the intestine is accompanied by reduced GIP release after intrajejunal glucose, depending on the degree of completeness of vagotomy.
Simultaneous 50-g oral glucose tolerance tests and measurements of gastric emptying time were performed in 11 duodenal ulcer patients. Gastric emptying time, measured by the gamma-camera technique, and the response of gastric inhibitory polypeptide (GIP) and enteroglucagon to the oral load showed a significant negative correlation. The GIP response and the insulinogenic index were significantly positively correlated. It is concluded that the increased GIP and insulin response to glucose among duodenal ulcer patients may be explained by increased gastric emptying, known to occur in these patients. The study has not given new information on the possible physiological role of enteroglucagon.
Ten male patients, recovered from acute myocardial infarction, and ten control subjects were investigated by a 50 g glucose tolerance test. All patients and control subjects had normal glucose tolerance, but the patients had increased fasting and integrated insulin response to oral glucose. Fasting gastric inhibitory polypeptide concentrations and integrated gastric inhibitory polypeptide response were normal in the patients. The exaggerated insulin secretion in patients recovered from myocardial infarction does not seem to be caused by increased secretion of gastric inhibitory polypeptide.
We previously showed that basal and pentagastrin-stimulated gastric acid secretion, gastrin in serum and gastrin in antral mucosa were significantly greater in patients with Roux-Y hepaticojejunostomy than in those with choledochoduodenostomy. These findings prompted investigation of basal secretion of gastric inhibitory polypeptide (a peptide with an enterogastrone as well as an insulinogenic effect), insulin and glucose in the same patients. Basal gastric inhibitory polypeptide was significantly lower in patients with Roux-Y hepaticojejunostomy than in those with choledochoduodensotomy, whereas glucose and insulin did not differ in the two groups. No correlation could be demonstrated between gastric inhibitory polypeptide, gastric acid secretion and gastrin, suggesting that hyposecretion of gastric inhibitory polypeptide is not a pathogenetic factor for the hypersecretion of gastric acid secretion in patients with Roux-Y hepaticojejunostomy. Hyposecretion of gastric inhibitory polypeptide and gastric acid hypersecretion in patients with bile diversion seem to be two independent phenomena.
The plasma concentrations of gastrin, gastric inhibitory polypeptide (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, glucagon, and pancreatic polypeptide (PP) were studied following the ingestion of a protein rich meal in late pregnancy and postpartum in 11 normal women. In pregnancy, the fasting plasma concentrations of glucose (mean +/- SEM in pregnancy: 4.1 +/- 0.1 mmol l-1, postpartum: 4.7 +/- 0.1 mmol l-1, P less than 0.01), gut GLI (25 +/- 3 v. 33 +/- 2 pmol-eqv l-1, P less than 0.01), and PP (7.9 +/- 1.0 v. 13.0 +/- 1.2 pmol l-1, P less than 0.01) were decreased, gastrin and GIP unaltered, and insulin (90 +/- 9 v. 72 +/- 5 pmol l-1, P less than 0.05) and glucagon (17 +/- 1 v. 13 +/- 1 pmol l-1, P less than 0.01) increased. The gastrin, GIP and glucagon responses to the meal were unaffected by pregnancy, whereas the responses of gut GLI (integrated responses in pregnancy: 1217 +/- 325 pmol-eqv l-1, postpartum 2223 +/- 404 pmol-eqv l-1, P less than 0.05) and PP (9801 +/- 1440 v. 14,078 +/- 1543 pmol l-1, P less than 0.01) were impaired and the insulin response enhanced (27,973 +/- 6814 v. 11,409 +/- 3102 pmol l-1, P less than 0.01) in pregnancy. The physiological implications of these findings are at present not known in detail. They may, however, be important for the altered carbohydrate metabolism in pregnancy and also for the changes occurring during gestation in gastrointestinal physiology.
The effect of gastric inhibitory polypeptide (GIP) in physiological concentrations (250, 500, 1,000 and 2,000 pg/ml) upon endocrine and exocrine secretion from the isolated perfused porcine pancreas was studied at various glucose concentrations in the perfusate. GIP increased insulin release in a dose-dependent manner. The sensitivity of the beta-cells to GIP was glucose independent. No effect was observed on glucagon or exocrine secretion regardless of the glucose concentration in the perfusate. We conclude that GIP is powerful insulin-stimulator even in low physiological concentrations in the presence of glucose concentrations comparable to those seen during an oral glucose load, which makes GIP to one of the strongest incretin candidates known, i.e. the factor(s) contributing to the augmented insulin response after ingestion of glucose.
The responses of gastric inhibitory polypeptides (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, and pancreatic glucagon to a 50-g oral glucose load were studied in late pregnancy and postpartum in 11 normal women, 10 normal weight gestational diabetics, and 10 overweight gestational diabetics. The GIP response to glucose was impaired in pregnancy in all three groups. In pregnancy, the GIP response was smaller in both groups of gestational diabetics than in normal women, whereas postpartum, the GIP response was lower than normal in the normal weight gestational diabetics only. In pregnancy, the gut GLI response to glucose was reduced in the overweight gestational diabetics and abolished in the normal women. The insulin response to glucose was increased in pregnancy in all three groups. Moreover, it was higher in the overweight gestational diabetics than in the other two groups in pregnancy and postpartum. In the normals, the suppression of glucagon levels after glucose ingestion was more marked in pregnancy than postpartum, whereas no such effect was seen in gestational-diabetic pregnancy. It is concluded that pregnancy--normal as well as gestational-diabetic--is accompanied by profound changes in the secretion of gastrointestinal insulinotropic hormones after glucose ingestion. These findings may be important for the understanding of changes in metabolism and gastrointestinal physiology in gestation.
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The serum or plasma concentrations of gastrin, gastric inhibitory polypeptide (GIP), gut glucagon-like-immunoreactivity (gut GLI), secretin, vasoactive intestinal polypeptide (VIP), insulin, glucagon, and pancreatic polypeptide (PP) were recorded simultaneously following the ingestion of a normal, mixed meal in seven healthy, normal weight men. The concentrations of PP and gastrin increased within 10 min. Subsequently GIP, insulin, glucagon, and gut GLI increased in the order mentioned. The mean concentrations of secretin and VIP were not affected by the meal, athough transient decreases in secretion concentrations could be detected in all subjects. The concentrations of the other hormones remained elevated for 4 hr or more. Perhaps the period of observation following food stimulation of gastro-entero-pancreatic hormones should be extended.