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Biomedical subjects

R Ebert

Publications and source records attributed to R Ebert.

At least 55 records · Page 3Linked to original sources
PubMed1989

[CO2-stunning of swine for slaughter from the anesthesiological viewpoint].

For investigations of CO2-stunning of feeder- and slaughter-pigs parameters of behaviour, blood-gas-analyses and electroencephalograms were chosen. The following results were obtained: 1. Blood-gas-analyses proved that the CO2-stunning does not produce unconsciousness due to a lack of oxygen. 2. The criterias of general anaesthesia: unconsciousness, muscle-relaxation and analgesia with total reversibility could be confirmed. 3. The violent convulsive symptoms were evaluated as reactions identical with the stage II of GUEDEL's scheme of anaesthesia. 4. Muscular agitation, which sometimes appeared a few seconds before the stage of excitation, was judged to belong either to the start of the excitation phase or to the end of Guedel's stage of analgesia, during which the sensitivity is decreased. Neither study of behavior nor objective measurements showed, during the first 10 to 20 seconds of exposure to the CO2, any sign of pain or suffering related to the Act for Prevention of Cruelty to Animals, and accordingly such suffering should not be ascribed to the CO2 stunning method.

Abattoirs↗
PubMed1988

Lack of insulinotropic effect of endogenous and exogenous cholecystokinin in man.

Intraduodenal phenylalanine administration (333 mg/min over 60 min) released endogenous cholecystokinin in healthy young subjects as demonstrated radioimmunologically and by intraduodenal bilirubin and pancreatic enzyme output. Concomitantly, there was only a small increase over basal in circulating immunoreactive-insulin and immunoreactive-C-peptide concentrations. In healthy volunteers intraduodenal infusions of saline (10 ml/min), glucose (333 mg/min) or phenylalanine (333 mg/min) were performed for 60 min when plasma glucose was clamped at approximately 8 mmol/l. Phenylalanine enhanced immunoreactive-insulin and immunoreactive-C-peptide responses three-fold more than did the same amount of glucose. Immuno-reactive gastric inhibitory polypeptide responses were small and not different after glucose and phenylalanine administration. Immunoreactive cholecystokinin was significantly stimulated to 9.4 +/- 1.4 pmol/l only by intraduodenal phenylalanine. Plasma phenylalanine concentrations increased into the supraphysiological range (approximately 1.5 mmol/l). Intravenous infusions of phenylalanine achieving plasma concentrations of 1.2 mmol/l stimulated insulin secretion at elevated plasma glucose concentrations (approximately 8 mmol/l clamp experiments), but had no effect at basal plasma glucose concentrations. A small increase in cholecystokinin also was observed. Intravenous infusions of synthetic sulphated cholecystokinin-8 leading to plasma concentrations in the upper postprandial range (8-12 pmol/l) did not augment the immunoreactive-insulin or immunoreactive-C-peptide levels during hyperglycaemic clamp experiments, in the absence or presence of elevated plasma phenylalanine concentrations. It is concluded that the augmentation of the glucose-induced insulin release by intraduodenal administration of phenylalanine cannot be related to cholecystokinin release, but rather is explained by the combined effects of elevated glucose and phenylalanine concentrations. In man, cholecystokinin does not augment insulin secretion caused by moderate hyperglycaemia, elevations of phenylalanine concentrations, or combinations thereof.

Adult↗
PubMed1988

Endocrine pancreatic function during atrophy of the exocrine gland.

Serum levels of glucose, insulin, and gastric inhibitory polypeptide (GIP) in response to intraduodenal and intravenous glucose loads have been examined in rats with exocrine pancreatic atrophy induced by feeding them a copper-deficient diet supplemented with D-penicillamine for 10-12 weeks. Whereas pancreatic weight and protein and trypsin content were drastically reduced as compared with pair-fed controls, insulin content was not significantly different between experimental (1.10 U) and control (1.40 U) rats. The intravenous glucose infusion was given in a dose (1.2 g/kg/h) simulating the glucose concentrations observed in response to an intraduodenal glucose load of 2.0 g/kg body weight. Both basal and stimulated insulin concentrations were lower in experimental animals as compared with controls. However, if the relative insulin response is considered, insulin secretion was almost identical in experimental and control animals. Both groups released significantly more insulin after intraduodenal glucose load than after intravenous glucose application. It is concluded that the entero-insular axis is intact in rats with exocrine pancreatic atrophy.

Animals↗
PubMed1988

'Entero-insular axis' and surgical trauma.

To study the optimal means of postoperative energy supply, three glucose loads (5 g, 15 g, 40 g) were given via the enteral or the parenteral route before and immediately after abdominal surgery. Pre- and post-operatively, glucose and insulin concentrations were strongly dose-related after both kinds of administration. But the postoperative insulin concentrations were higher than the preoperative ones. Likewise, in both test situations the 'insulinogenic index' was significantly higher postoperatively than preoperatively. After the enteral glucose load, however, the index was 3 to 10 times higher than after the parenteral one. According to these results, even in the early postoperative period the enteral route of glucose administration is not only feasible but seems also to be superior to the parenteral one.

Adult↗
PubMed1988

Control of gastric emptying by regulatory peptides.

The rate of gastric emptying is controlled by humoral and nerval factors. When glucose, fat, or amino come into contact with the duodenal mucosa inhibitory mechanisms decrease the fundic pressure and thereby slow the gastric emptying of nutrients. Among the various peptides, so far investigated, gastrin inhibits the emptying rate, however, this effect is only seen at unphysiological high concentrations. Cholecystokinin, on the other hand, is able to decrease the delivery of glucose to the duodenum at physiological concentrations. Also secretin exerts an inhibitory effect on gastric emptying. The peptide YY which is released from the ileum and colon after ingestion of carbohydrates or fat and which inhibits gastric acid secretion also reduces the amount of food emptied from the stomach. This inhibitory effect was achieved by doses which are within the physiological range. The neuropeptide vasoactive intestinal polypeptide (VIP) and the enkephalins are both able to retard the gastric emptying. Some of these effects, especially of VIP, are mediated by noncholinergic, non-adrenergic inhibitory vagal nerves. Stimulation of gastric emptying is seen with motilin and somatostatin. The effect of motilin is a direct one, whereas the effect of somatostatin is probably due to inhibition of regulatory peptides which in turn inhibit the emptying in the sense of a feedback. So far, these peptides which are responsible for the inhibitory effect of gastric emptying following the presence of carbohydrates in the duodenum, have not yet been elucidated. The rate of glucose delivery to the duodenum determines the shape of the blood glucose curve and either directly via the blood glucose or indirectly via the release of insulinotropic gut hormones, also the amount of insulin secreted.

Animals↗
PubMed1988

Effects of single and combined infusions of human biosynthetic proinsulin and insulin on glucose metabolism and on plasma hormone concentrations in euglycaemic clamp experiments.

Euglycaemic clamp experiments with single or combined infusions of human biosynthetic proinsulin and insulin were performed in 6 healthy, normal weight subjects in order to assess the possibility of antagonistic, additive, or synergistic effects on whole body glucose metabolism. Insulin (i: 2.02 pmol x kg-1 x min-1) or proinsulin (p: 9.26 pmol x kg-1 x min-1) were infused under euglycaemic clamp conditions over 240 min. After 120 min, the infusion rates were doubled (protocols ii and pp), or proinsulin (protocol ip) or insulin (protocol pi) infusions were added. After 240 min of infusing insulin or proinsulin alone, euglycaemia was maintained for an additional 60 min period without hormone infusions to measure the decay of hormone concentrations and of effects on glucose metabolism. Effects on glucose uptake were measured as the glucose infusion rate necessary to maintain euglycaemia. IR-insulin, IR-proinsulin, IR-C-peptide and IR-glucagon were determined by specific radioimmunoassays. After 240 min, similar steady state glucose infusion rates were reached for all protocols (mean +/- SEM, mg x kg-1 x min-1: ii: 10.6 +/- 1.0; ip: 9.1 +/- 0.4; pi: 10.0 +/- 0.9; pp: 8.4 +/- 0.7). The infusion rate with proinsulin alone (pp), however, was significantly smaller than with insulin alone (ii), indicating a somewhat lower effectiveness of the proinsulin dose employed. With all protocols, nonesterified fatty acid and IR-glucagon concentrations were decreased to a similar extent. Steady state hormone concentrations were reached within 30 min of each infusion period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Isotopically sensitive branching in the formation of cyclic monoterpenes: proof that (-)-alpha-pinene and (-)-beta-pinene are synthesized by the same monoterpene cyclase via deprotonation of a common intermediate.

To determine whether the bicyclic monoterpene olefins (-)-alpha-pinene and (-)-beta-pinene arise biosynthetically from the same monoterpene cyclase by alternate deprotonations of a common carbocationic intermediate, the product distributions arising from the acyclic precursor [10-2H3,1-3H]geranyl pyrophosphate were compared with those resulting from incubation of [1-3H]geranyl pyrophosphate with (-)-pinene cyclase from Salvia officinalis. Alteration in proportions of the olefinic products generated by the partially purified pinene cyclase resulted from the suppression of the formation of (-)-beta-pinene (C10 deprotonation) by a primary deuterium isotope effect with a compensating stimulation of the formation of (-)-alpha-pinene (C4 deprotonation). (-)-Pinene cyclase as well as (+)-pinene cyclase also exhibited a decrease in the proportion of the acyclic olefin myrcene generated from the deuteriated substrate, accompanied by a corresponding increase in the commitment to cyclized products. The observation of isotopically sensitive branching, in conjunction with quantitation of the magnitude of the secondary deuterium isotope effect on the overall rate of product formation by the (+)- and (-)-pinene cyclases as well as two other monoterpene cyclases from the same tissue, supports the biosynthetic origin of (-)-alpha-pinene and (-)-beta-pinene by alternative deprotonations of a common enzymatic intermediate. A biogenetic scheme consistent with these results is presented, and alternate proposals for the origin of the pinenes are addressed.

Bicyclic Monoterpenes↗
PubMed1987

Effect of the somatostatin analogue sandostatin (SMS 201-995) on gastrointestinal, pancreatic and biliary function and hormone release in normal men.

The effect of the long-acting somatostatin analogue Sandostatin (SMS 201-995) on intestinal absorption and propagation (mouth-to-caecum transit time; MCTT), on pancreatic secretion and on gall bladder contraction after direct (secretin-pancreozymin test) and indirect stimulation (Lundh meal), and on meal-induced responses of seven gastrointestinal regulatory peptides has been investigated. In a double-blind cross-over study, 9 healthy volunteers completed two 7-day periods with subcutaneous injections of either placebo or 25 micrograms SMS 201-995 twice daily. Mean faecal fat excretion was increased to 19.2 g/day and MCTT was three times longer during the SMS period. After duodenal infusion of a mixture containing D-galactose, D-xylose and triglycerides, SMS 201-995 significantly reduced the serum concentrations of D-galactose but increased serum levels of D-xylose. After 6 days of pretreatment, SMS 201-995 completely suppressed duodenal trypsin, lipase and bilirubin increases in response to endogenous stimulation by a Lundh meal. Concomitantly, cholecystokinin (CCK) release and gall bladder contraction were almost abolished. Compared with placebo, SMS 201-995 significantly diminished pancreatic amylase, trypsin and lipase output after stimulation with CCK, while the secretion of fluid and bicarbonate in response to secretin was unchanged. This inhibition of enzyme response was significantly more marked after a single injection of the analogue than after pretreatment for 7 days and did not reach the level of exocrine pancreatic insufficiency. CCK-induced gall bladder contraction was significantly inhibited by a single dose of 25 micrograms SMS 201-995 but not after 7 days of pretreatment with the somatostatin analogue.

Adult↗
PubMed1986

Insulin-dependent inhibition of hepatic glycogenolysis by gastric inhibitory polypeptide (GIP) in perfused rat liver.

The effect of porcine gastric inhibitory polypeptide on hepatic glycogen metabolism was investigated in the isolated in situ perfused rat liver. Glycogenolysis was stimulated by infusion of glucagon into the portal vein (half maximal effective portal vein concentration approximately 30 pmol/l). When glucagon was infused at a final portal vein concentration of 0.5 nmol/l, simultaneous addition of insulin inhibited the glucagon-dependent glycogenolysis in a dose-dependent way (half maximal effective concentration for insulin about 2 nmol/l). Gastric inhibitory polypeptide alone at a concentration of 1 nmol/l reduced glucagon-dependent glycogenolysis only slightly. However, when infused simultaneously at low insulin concentrations (0.1 nmol/l), gastric inhibitory polypeptide suppressed hepatic glucose production dose-dependently up to 70%. The data suggest that gastric inhibitory polypeptide exerts direct metabolic effects on hepatic glycogen metabolism predominantly in a situation where insulin is simultaneously present, e.g. following ingestion of glucose.

Animals↗
PubMed1986

Comparison of gastric inhibitory polypeptide and intraduodenal or intravenous fat on gastric acid secretion from vagally innervated and denervated canine stomach.

Gastric inhibitory polypeptide (GIP), given to dogs in graded doses (range 0.25-2 micrograms/kg/hr) against a constant background stimulation with pentagastrin (4 micrograms/kg/hr), failed to affect the acid secretion at all doses used except the largest one (2 micrograms/kg/hr) which significantly reduced the acid secretion only from the vagally denervated portion of the stomach (Heidenhain pouch, HP) while raising plasma GIP two to three times above the levels reached with duodenal fat. GIP infused in a constant dose (1 microgram/kg/hr) significantly reduced the HP responses to lower (0.5-2 micrograms/kg/hr) but not to higher (4-16 micrograms/kg/hr) doses of pentagastrin, the kinetics of this inhibition being of competitive type. GIP was ineffective against a constant near maximal stimulation with pentagastrin (4 micrograms/kg/hr), histamine (40 micrograms/kg/hr), or liver extract meal, whereas fat (10 g), given intraduodenally or intravenously, was a powerful inhibitor of acid responses to these stimulants both from the innervated and denervated stomach. Plasma GIP reached similar levels with exogenous GIP and duodenal fat but remained unchanged with intravenous infusion of fat.

Animals↗
PubMed1986

Reduced incretin effect in type 2 (non-insulin-dependent) diabetes.

Integrated incremental immunoreactive insulin and connecting peptide responses to an oral glucose load of 50 g and an "isoglycaemic" intravenous glucose infusion, respectively, were measured in 14 Type 2 (non-insulin-dependent) diabetic patients and 8 age- and weight-matched metabolically healthy control subjects. Differences between responses to oral and intravenous glucose administration are attributed to factors other than glucose itself (incretin effect). Despite higher glucose increases, immunoreactive insulin and connecting peptide responses after oral glucose were delayed in diabetic patients. Integrated responses were not significantly different between both groups. However, during "isoglycaemic" intravenous infusion, insulin and connecting peptide responses were greater in diabetic patients than in control subjects as a consequence of the higher glycaemic stimulus. The contribution of incretin factors to total insulin responses was 72.8 +/- 6.9% (100% = response to oral load) in control subjects and 36.0 +/- 8.8% in diabetic patients (p less than or equal to 0.05). The contribution to connecting peptide responses was 58.4 +/- 7.6% in control subjects and 7.6 +/- 14.5% (p less than or equal to 0.05) in diabetic patients. Ratios of integrated insulin to connecting peptide responses suggest a reduced (hepatic) insulin extraction in control subjects after oral as compared to intravenous glucose. This was not the case in diabetic patients. Immunoreactive gastric inhibitory polypeptide responses were not different between control subjects and diabetic patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Gastric inhibitory polypeptide and insulin response to increasing doses of oral glucose: dependency on glucose amount and volume of the test drink.

The plasma levels of glucose, immunoreactive insulin (IRI), and immunoreactive GIP (IR-GIP) of eight healthy normal-weight subjects were compared following administration of oral glucose load of 10, 30, 60, 90, and 120 g, each given in a volume of 300 and 600 mL of water. By increasing the glucose load from 30 to 60 g, the integrated glucose response was more than doubled, irrespective of the volume. If more than 60 g glucose was given, the venous blood glucose levels did not significantly increase further. The IRI concentrations peaked between 30 and 40 minutes, irrespective of the size and volume of the glucose load. The peak values were significantly higher if 30, 60, and 90 g glucose was given in 600 mL than in 300 mL water. The integrated IRI output increased gradually if the glucose concentration of the 300 mL load was increased, whereas a maximal IRI response occurred already with 60 g glucose if dissolved in 600 mL water. At identical amounts of glucose (60 g) the integrated IRI response was doubled by increasing the ingested volume of the drink from 300 to 600 mL. Also the peak and integrated IR-GIP response increased in a dose-dependent manner by increasing the size of the glucose load. Larger amounts of glucose mainly prolong the GIP response. Significantly greater amounts of IR-GIP were released with 60 and 90 g glucose when given in 600 mL instead of 300 mL water. The parallel increment of IR-GIP and IRI is compatible with an important role of GIP as an insulinotropic gut factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1986

Incretin effects of increasing glucose loads in man calculated from venous insulin and C-peptide responses.

Integrated insulin secretion rates calculated from peripheral venous C-peptide measurements by two-compartment kinetic analysis were measured in six young normal subjects after increasing oral glucose loads of 25, 50, and 100 g and respective isoglycemic glucose infusions. The differences in B-cell secretory responses between oral and iv glucose challenges were attributed to factors other than glycemia itself (incretin effect). Both insulin and C-peptide concentrations as well as calculated integrated insulin secretion rates increased with increasing oral glucose loads. Due to the similarity in the glucose profiles after all oral loads, almost identical amounts of iv glucose (approximately 20 g) were infused in all "isoglycemic" infusion experiments, with resulting similar hormone profiles and insulin secretion rates. The percent contribution of incretin factors to total immunoreactive insulin responses after 25, 50, and 100 g glucose (85.6%, 74.9%, and 93.0%; response to oral load, 100%) was significantly higher than their contribution to integrated C-peptide responses (27.6-62.9%) or calculated integrated insulin secretion rates (19.2-61.0%). These findings indicate that the degree of incretin stimulation of insulin secretion depends on the amount of glucose ingested. A discrepancy between the estimates of the incretin effect derived from peripheral venous insulin responses, on the one hand, and C-peptide responses or calculated insulin secretion rates, on the other hand, exists. Inasmuch as peripheral insulin values reflect both insulin secretion and hepatic insulin removal, this discrepancy suggests that elimination kinetics of insulin differ between oral and iv glucose administration. This difference can be related to a significantly reduced fractional hepatic insulin extraction after oral (46.9-54.6%) compared to iv (63.4-76.5%) glucose administration when calculated by a three-compartment kinetic model. This reduction in fractional hepatic insulin extraction could be caused by gastrointestinal factors (hormones or nerves) stimulated in the course of glucose ingestion.

Administration, Oral↗