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Biomedical subjects

R Ebert

Publications and source records attributed to R Ebert.

At least 73 records · Page 4Linked to original sources
PubMed1983

GIP and insulin responses to a test meal in healthy and obese subjects.

Twenty-three obese and 17 control subjects were studied after ingestion of a heavy breakfast. Blood samples were drawn before and at 30, 60, 90, 120, 150, and 180 min after the start of the meal. The m ean serum insulin level was significantly (p less than 0.02) higher in the obese than in the control group throughout the study, whereas the mean blood glucose concentration was significantly (p less than 0.02) higher in the obese group at 30, 60, and 90 min only. No significant differences between the two groups were noted in fasting or in postprandial plasma GIP, and it appears that hypersecretion of GIP is not responsible for the hyperinsulinemia seen in obesity.

Adult↗
PubMed1983

Disturbances of the entero-insular axis.

The entero-insular axis comprises direct substrate stimulation of the islet cells by the absorbed nutrients and signal transmission by endocrine factors and nerves. The extent of neural influences has not yet been evaluated. GIP is the main incretin candidate. GIP release is dependent on nutrient absorption. Therefore, GIP abnormalities occur in a large number of gastrointestinal and metabolic diseases. These secondary changes are rarely of clinical significance. GIP hypersecretion may, however, contribute to the increased lipogenesis in obesity and the hypoglycemia in the late dumping syndrome. In type II diabetes hyper- and hyposecretion of GIP has been found but no correlation between GIP and insulin response. GIP abnormalities are not identical with disturbances of the entero-insular axis. These can only be evaluated by estimating the incretin effect (comparing the insulin response to oral glucose with the insulin response to an isoglycaemic iv glucose infusion). A decreased incretin effect has been observed in patients with jejuno-ileal bypass and in type II diabetes. In neither condition was a correlation found between incretin effect and GIP response. It is concluded that disturbances of the entero-insular axis are rarely explained by GIP abnormalities. Therefore, other humoral gut factors must exist. Also the neural part of the entero-insular axis requires exploration in health and disease.

Animals↗
PubMed1982

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↗
PubMed1982

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↗
PubMed1982

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↗
PubMed1982

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↗
PubMed1982

[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↗
PubMed1981

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↗
PubMed1981

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↗
PubMed1980

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↗
PubMed1980

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↗
PubMed1980

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↗
PubMed1980

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↗