[Development of employment-induced hearing loss caused by noise in the district of Halle 1971-1981].
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Germany, East↗
Biomedical subjects
R Ebert
Publications and source records attributed to R Ebert.
Adrenergic modulation of gastric inhibitory polypeptide secretion in man.
In order to examine the effect of adrenergic influences on gastric inhibitory polypeptide (GIP) secretion, a series of glucose tolerance tests was carried out in seven healthy volunteers during intravenous infusion of epinephrine (6 microgram/min), epinephrine plus phentolamine (5 mg stat + 0.5 mg/min), epinephrine plus propranolol (5 mg stat + 0.08 mg/min), and saline. No drug infusion modified fasting GIP levels. Alpha-adrenergic stimulation (epinephrine + propranolol) significantly reduced the GIP response (P less than 0.02) and completely inhibited the insulin response (P less than 0.005) to oral glucose, compared with control experiments. Epinephrine alone and epinephrine + phentolamine did not influence glucose-stimulated GIP. These results suggest the possibility that the adrenergic nervous system may have a role in the regulation of GIP secretion in man.
Adult↗
Betazole-induced GIP secretion is not mediated by gastric HCl.
Betazole, a pyrazole analogue of histamine, as well as pentagastrin and HCl stimulate GIP secretion. We have asked the question as to whether betazole acts directly or via the production of HCl. Eight normal subjects and 4 patients with achlorhydria secondary to pernicious anemia were given betazole (0.5 mg/kg) by IM injection. Another six normal subjects were also given betazole but this was preceded by 200 mgs. of the H2 receptor blocker cimetidine given IV 60 mins. previously and a slow infusion of 200 mg. cimetidine given over the next 4 hr. Our results have shown that the GIP response to betazole is maintained in achlorhydric subjects as well as during H2 blockade. The results suggest that betazole and therefore histamine may stimulate GIP directly and not necessarily via the mediation of HCl.
Achlorhydria↗
Influence of metronidazole on the breath hydrogen response and symptoms in acarbose-induced malabsorption of sucrose.
The influence of metronidazole on the breath hydrogen response and symptoms of sucrose malabsorption was investigated in a double-blind, randomized and controlled study. Carbohydrate malabsorption was induced by the competitive alpha-glucosidase inhibitor, acarbose. Metronidazole reduced flatulence and the breath hydrogen response during sucrose malabsorption without a change in intestinal carbohydrate absorption, as indicated by serum levels of gastric inhibitory polypeptide, serum insulin and blood glucose. The effect of metronidazole suggests that anaerobic bacteria mediate both signs and symptoms of the colonic response to sucrose malabsorption. In contrast to previous reports on lactose malabsorption, it was not possible to quantify sucrose malabsorption by comparing the breath hydrogen response to sucrose malabsorption with the H2 response to a lactulose load.
Acarbose↗
Influence of gastric inhibitory polypeptide antiserum on glucose-induced insulin secretion in rats.
The action of gastric inhibitory polypeptide (GIP) antiserum on glucose tolerance and insulin secretion after an intraduodenal glucose load (600 mg/kg) was examined in anesthetized rats. In control experiments the insulin secretion was nearly doubled when glucose was administered intraduodenally, as compared to an iv glucose load to simulate the blood glucose curve after the intraduodenal glucose administration. After injection of GIP antiserum, the glucose curve resulting from the intraduodenal glucose load was slightly elevated and the insulin response was significantly reduced. No free GIP could be measured in the plasma of antibody-treated rats. However, the GIP antiserum did not offset the incretin effect of the intraduodenal glucose load completely. In control experiments the same amount of GIP antibody completely blocked the insulinotropic effect of exogenous porcine GIP (0.6 microgram/kg . h). In nonanesthetized rats serial oral glucose tolerance tests were performed for 14 days after injection of the GIP antiserum. Despite the blockage of endogenous GIP, the glucose tolerance did not change significantly in the antibody-treated group of rats as compared to a control group. These data indicate that GIP is not the exclusive incretin and that additional gut factors with insulinotropic activity exist.
Animals↗
[Biochemical changes with continuous ambulant peritoneal dialysis (CAPD)].
During the past few years continuous ambulatory peritoneal dialysis (CAPD) has become well established in the home treatment of uremia. CAPD, however, may induce certain biochemical abnormalities. Using glucose as an osmotic agent of the dialysate the peritoneal glucose load may vary between 75 and 200 g per day, depending upon how often high osmotic dialysate is needed. If the latter is restricted to one bag per day a long-term disturbance of the glucoregulatory hormones insulin, GIP an glucagon seem to be inprobable. Investigations into glucose tolerance after 23 til 34 months of CAPD treatment in 4 patients did not indicate any exhaustion of the pancreatic beta-cells. Long-term evaluation into the metabolism of lipoproteins, total plasma proteins, aminoacids and trace elements did not show significant abnormalities induced by CAPD itself. Biochemical alterations observed are more or less related to the uremic state of the patients.
Adult↗
[Problems of work hygiene in a newly founded town].
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Female↗
Effect of exogenous insulin on fasting serum levels of gastric inhibitory polypeptide (GIP) in juvenile diabetes.
The effect of insulin on fasting levels of immunoreactive gastric inhibitory polypeptide (IR-GIP) has been examined in insulin-dependent, juvenile-type diabetics who were well-controlled with two doses of an intermediate insulin. After withdrawal of the evening insulin injection the fasting blood glucose and serum IR-GIP levels were elevated and decreased significantly following intravenous insulin towards normal values. There was a significant positive correlation between levels of blood glucose and serum IR-GIP before and during insulin application. It is suggested that fasting serum GIP levels increase in case of insulin deficiency because basal GIP secretion is suppressed by normal insulin levels.
Adult↗
Response of serum levels of gastric inhibitory polypeptide and insulin to sucrose ingestion during long-term application of acarbose.
Sucrose (100 g) loading tests were performed in 10 healthy volunteers before and during the intake of an alpha-glucosidehydrolase inhibitor (acarbose) for 8 weeks (3 X 200 mg daily) and serum levels of glucose, immunoreactive insulin (IRI), and immunoreactive gastric inhibitory polypeptide (IR-GIP) were measured. The addition of 200 mg of acarbose to the sucrose load attenuated the sucrose-induced glycaemia and IRI response and completely abolished the IR-GIP release. The volunteers complained about meteorism and abdominal pain during the intake of the inhibitor. These side effects became less marked at the end of the study. The attenuation of complaints cannot be explained by a decreasing sucrase inhibition, since the increase of glucose, IRI, and IR-GIP after sucrose loading at the beginning and after 4 and 8 weeks was equally impaired by acarbose.
Acarbose↗
Plasma and urine concentrations of acebutolol and its acetyl metabolite in patients with renal functional impairment.
This study was undertaken to examine the elimination of orally administered acebutolol and its major acetyl metabolite in four healthy controls and seven patients with varying degrees of renal functional impairment. Analysis of acebutolol and its metabolites was undertaken using a high performance liquid chromatographic method. Plasma concentrations of acebutolol and the acetyl metabolite were greater in patients with renal functional impairment than in controls. The elimination of acebutolol did not appear to be influenced by impaired renal function. However the elimination of the acetyl metabolite decreased as renal function diminished. Acebutolol has a major non-renal route of elimination, but the acetyl metabolite (also a beta-adrenoreceptor blocking drug) is primarily excreted by the kidney and may accumulate in renal failure.
Acebutolol↗
Reversal of impaired GIP and insulin secretion in patients with pancreatogenic steatorrhea following enzyme substitution.
The influence of impaired digestion on nutrient induced release of gastric inhibitory polypeptide (GIP) and insulin have been investigated in patients with chronic pancreatitis. All patients had massive steatorrhea (> 25 g/24 h), and glucose intolerance. A standard liquid test meal comprising fat and glucose were ingested with or without pancreatic enzyme substitution (9.0 g pancreatin). In the presence of pancreatin the response of serum levels of GIP to the test meal was significantly enhanced (81.2 vs 194.5 microgram/l X 180 min). Concurrently, the insulin response was augmented (3.4 vs 6.4 U/l X 180 min), resulting in improved glucose tolerance. Addition of pancreatin also significantly augmented the GIP response to oral fat (100 g), but not to oral glucose (100 g). In patients with pancreatogenic steatorrhea the insulin response to an IV glucose infusion (0.7 g/kg/h for 90 min) was augmented by oral fat only after addition of 9.0 g pancreatin to the fat load (3.5 vs 7.3 U/l X 180 min). After restoration of the GIP response to fat by pancreatin, the inhibitory effect of IV glucose on fat-induced GIP increase was restored. These data indicate that the GIP response to a mixed meal or triglycerides is dependent on the absorption of nutrients. In patients with chronic pancreatitis improvement of pancreatogenic insufficiency reverses the impaired GIP response, restores the incretin effect of fat, and improves glucose tolerance.
Adult↗
Acid-induced gastric inhibitory polypeptide secretion in man.
This study has assessed the effect of oral or intraduodenal HCl, administered alone or in combination with glucose, on gastric inhibitory polypeptide (GIP) and insulin secretion. Eight young males were given the following three oral tests: 30 g glucose, 150 cc 0.1 N HCl and the glucose-acid combination. Another group of eight controls received intraduodenal infusions of 20 g glucose, 75 cc 0.1 N HCl and their combination. All tests were performed in a random fashion at weekly intervals. When given alone, HCl did not influence glucose or insulin levels. However, HCl did produce an increase in GIP. The GIP response to acid was less than that to glucose and was delayed. The peak insulin and GIP responses with the glucose and glucose/acid combinations were similar with both the oral and intraduodenal routes. There was, however, a potentiation of both the GIP and insulin responses when intraduodenal acid was given with glucose. This effect on GIP and insulin was not evident with the oral glucose/acid load. It is concluded that HCl by itself is capable of stimulating GIP secretion. Since there was only a potentiation of insulin and GIP secretion when large doses of HCl were given together with glucose via the intraduodenal route, the physiological relevance of acid-induced GIP secretion remains to be resolved.
Administration, Oral↗
[Application of ceramics in spare parts surgery (author's transl)].
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Ceramics↗
Inhibition of gastric inhibitory polypeptide (GIP) release by insulin and glucose in juvenile diabetes.
The effect of glucose and insulin on fat- and glucose-induced gastric inhibitory polypeptide (GIP) release has been studied in insulin-dependent juvenile-type diabetics. Blood glucose and serum immunoreactive GIP (IR-GIP) were measured after an oral load of 100 g glucose or 100 g fat was given and during an infusion of one of the following: saline, glucose, glucose plus insulin, or insulin. The infusion of insulin alone (in the presence of elevated glucose levels) or together with glucose significantly suppressed the IR-GIP rise after fat ingestion, but it did not alter the GIP response to oral glucose. Intravenous infusion of glucose had a slight but significant inhibitory effect on fat-stimulated increase of IR-GIP, which cannot be related to endogenous insulin release in these insulin-deficient diabetics. It is suggested that an insulin-mediated increase of glucose utilization in the GIP cell interferes only with increased GIP secretion stimulated by the utilization of fatty acids but not of glucose. This could explain the existence of a negative feedback control between insulin and GIP secretion for fat but not for glucose-induced GIP release.
Adult↗
Gastric inhibitory polypeptide.
The available data show that GIP is at present the strongest candidate for the insulin-secreting factor of the gut named incretin. Its release is triggered by the absorption of ingested nutrients. GIP acts on the B-cells of the pancreas by potentiating glucose-induced insulin secretion. The role of GIP as an enterogastrone is less well established. The release of GIP from the gut cells seems to be regulated by the composition and the amount of the ingested food, by the rate of absorption of nutrients by neural factors (vagal), and by feedback control mediated by insulin. In addition, the adaptation of the intestine to individual eating habits influences the response of the GIP cells. It is suggested that an overactive enteroinsular axis, i.e. enhanced GIP secretion, participates in the development of the hyperinsulinaemia of obesity and maturity onset diabetes mellitus. In gastrointestinal diseases accompanied by malabsorption the GIP response is diminished. In gastrointestinal disorders with rapid gastric emptying (duodenal ulcer) or with accelerated passage of the nutrients through the intestine, hypersecretion of GIP and insulin occurs. This may be significant for the reactive hypoglycaemia of these conditions.
Adolescent↗
Biochemical investigations of CAPD: plasma levels of trace elements and amino acids and impaired glucose tolerance during the course of treatment.
Investigations have been initiated into the effect of CAPD on the plasma concentrations of trace elements and amino acids, and in particular the response of patients to an oral glucose tolerance test (OGTT) during the course of treatment. Six months CAPD had no effect on the plasma concentrations of aluminium, fluoride, zinc and copper. Levels of aluminium and fluoride were above the normal range. Loss of amino acids in the dialysate correlated with their plasma concentrations. No changes were observed in the E/NE, Val/Gly or Tyr/Phe ratios during nine months treatment. Five CAPD patients demonstrated an impaired glucose tolerance in response to an OGTT after one month of treatment and a further deterioration occurred in the glucose tolerance of three patients after another six months CAPD. In a preliminary investigation with fructose substituted for glucose in the dialysate of one patient, an improvement in the OGTT and rate of insulin secretion was observed after 3 days dialysis against fructose.
Adolescent↗
Impaired feedback control of fat induced gastric inhibitory polypeptide (GIP) secretion by insulin in obesity and glucose intolerance.
To investigate the role of endogenous insulin on the secretion of immunoreactive gastric inhibitory polypeptide (IR-GIP) the response of IR-GIP and immunoreactive insulin (IRI) to an oral fat load (100 g triglyceride) alone and during an intravenous glucose infusion (0.7 g/kg/h) was examined in normal weight and obese subjects. In normal weight subjects the fat induced integrated rise of IR-GIP was 112.7 +/- 9.4 ng/ml/120 min. When glucose and fat were given together this IR-GIP response was lowered to 46.2 +/- 2.9 ng/ml/120 min while the serum IRI response to i.v. glucose and the glucose tolerance were enhanced by fat ingestion. In obese subjects with normal glucose tolerance the GIP suppressing effect of i.v. glucose infusion was less marked than in controls. The integrated IR-GIP response to fat ingestion was 225.6 +/- 20.3 mg/ml/120 min and to fat plus glucose 152.6 +/- 14.8 ng/ml/120 min. In obese subjects with glucose intolerance i.v. glucose completely failed to lower the exaggerated secretion of IR-GIP following oral fat. Thus, a graded abnormality of the GIP response to glucose induced insulin release occurs in obesity with normal and pathological glucose tolerance. After reducing the ideal body weight of six obese subjects with glucose intolerance by hypocaloric diet for 3 weeks the exaggerated rise of IR-GIP after oral fat was reversed and the lowering effect of i.v. glucose on the IR-GIP response re-established.
Adult↗