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Biomedical subjects

R Jorde

Publications and source records attributed to R Jorde.

At least 145 records · Page 8Linked to original sources
PubMed1982

Fasting and diurnal plasma PP, and the effect of fasting and somatostatin on postprandial plasma PP.

6 healthy subjects were studied on 3 separate occasions after ingestion of an ordinary breakfast. Once the meal was given alone, once together with somatostatin infused i.v. (100 micrograms/h) for the first 2 h after start of the meal, and once the meal was preceded by a 34-h fasting period. The postprandial plasma PP secretion was completely inhibited during the somatostatin infusion, and significantly augmented (p = 0.032) after the prolonged fast. During the 34-h fasting period, the PP levels were almost unaffected. The same group of subjects were also studied during a "normal" day with 4 regular meals. Plasma PP was found to increase shortly after breakfast and did not return to basal levels before early the next morning. The integrated PP secretion during the 24-h period showed a significant (p less than 0.003) correlation with the basal levels.

Adult↗
PubMed1982

Iodination with Iodo-gen and radioimmunoassay of cholecystokinin (CCK) in acidified plasma, CCK release, and molecular CCK components in man.

The preparation of a stable fully immunoreactive 125I-labeled CCK39 using a modified Iodo-gen method with high specific radioactivity; the production of an avid and specific cholecystokinin (CCK) antiserum, and a sensitive, precise and specific radioimmunoassay method allowing measurements of fasting plasma CCK in the low picomole per liter range together with the significant rises in plasma CCK following a test meal and duodenal infusion of fat are described. Apparent immunoreactive fasting plasma CCK was eluted from a Sephadex G-50 Fine column in one peak probably representing plasma CCK bound to plasma proteins and nonspecific plasma effects. Apparent immunoreactive postprandial plasma CCK was eluted from a Sephadex G-50 Fine column in four peaks. The first peak probably represents plasma CCK bound to plasma proteins and nonspecific plasma effects; the second peak probably represents component I with a molecular weight between some 5,000 and 30,000; the third peak probably represents component II or CCK33, and the fourth peak probably represents component IV or CCK8.

Adult↗
PubMed1982

Effect of gastrin on fasting and postprandial plasma GIP release in man.

In order to evaluate the mechanism behind the augmented postprandial gastric inhibitory polypeptide (GIP) release seen in patients with achlorhydria and hypergastrinemia, 8 healthy subjects were given a liquid test meal on three different days. On 1 day the meal was preceded by ranitidine (H2 receptor antagonist) to block the gastric H+ secretion. On another day the meal was also preceded by ranitidine, but on this occasion gastrin was infused intravenously during the first hour in order to induce hypergastrinemia. On a third day the meal was given along to serve as a control. Finally, 6 healthy fasting subjects were given a 1-hour intravenous infusion of gastrin after pretreatment with ranitidine. Plasma GIP responses after the meal on the days with ranitidine alone or together with the gastrin infusion did not differ significantly from that found on the control day. When gastrin was infused in the fasting state, no effect was seen on the basal GIP levels. Thus, neither exogenous gastrin nor achlorhydria seems to affect the plasma GIP release, and it appears more likely that a rapid gastric emptying rate can account for the augmented GIP response found in achlorhydric patients.

Adult↗
PubMed1982

Effect of jejunoileal bypass operation and Billroth II resection on postprandial plasma pancreatic polypeptide release.

In five jejunoileal bypass-opeated subjects mean plasma pancreatic polypeptide (PP) values were significantly higher 15, 30, and 60 min. after start of a meal 2 weeks postoperatively, and 15 min. after start of a meal 6 weeks postoperatively, as compared with preoperative values. In a group of eight obese subjects, operated on with jejunoileal bypass 2-5 years ago, the postprandial plasma PP release tended to be higher than in an age-matched control group, the difference, however, being significant at 15 min. only. On the other hand, the postprandial plasma PP release in a group of six Billroth-II-resected patients was almost identical to that seen in an age-matched control group. It appears as though neither the antrum nor the small intestine is a prerequisite for a normal PP response to a mixed liquid test meal.

Adult↗
PubMed1982

Duodenal acid is without importance for the postprandial PP release.

In six healthy subjects duodenal infusion of 30 ml 100 mmol/1 HCl caused a slight, but significant, release of plasma pancreatic polypeptide (PP), whereas infusion of 3 g dried cattle bile dissolved in 30 ml distilled water did not affect basal plasma PP levels. In another group of six healthy subjects the postprandial plasma PP release was not affected by inhibition of the gastric H+ secretion by the H2-receptor antagonist ranitidine. Finally, the meal-induced plasma PP release in a group of 19 achlorhydric patients did not differ significantly from that seen in 11 normal controls. We therefore conclude that, although duodenal acidification may elicit release of plasma PP, gastric H+ secretion seems to be without importance for the postprandial plasma PP release.

Achlorhydria↗
PubMed1982

Renal excretion of and the effect of posture on serum group I pepsinogens.

Serum group I pepsinogens (PG I) were determined by a radioimmunoassay method in blood drawn from the right femoral vein, the right renal vein, the liver vein, the right atrium, and the left femoral artery from 10 patients undergoing cardiac catheterization. Clinically they had no cardiac insufficiency, and their renal function was normal. The serum PG I concentration was similar in the femoral artery and vein and in the right atrium. On the other hand, serum PG I was higher in the liver vein and lower in the renal vein than in the other sampling sites. The renal arteriovenous serum PG I difference was positively correlated to the arterial concentration. The influence of posture on serum PG I was studied in another nine healthy subjects. Serum PG I was lower in the supine position than in the erect position.

Adolescent↗
PubMed1982

Augmented release of gastric inhibitory polypeptide into the portal vein in response to intraduodenal glucose and amino acids in anesthetized rats treated with methylprednisolone or alloxan.

Thirty rats were treated with methylprednisolone, 30 rats were treated with alloxan, and 30 control rats were treated with saline alone. The levels of fasting serum insulin and blood glucose and of plasma GIP before and after duodenal instillation of glucose or amino acids were measured using an acute rat preparation that enabled multiple blood samplings from the portal vein. Treatment of the rats with methylprednisolone was followed by increased fasting levels of serum insulin, blood glucose, and plasma GIP and by an augmented GIP release in response to duodenal glucose and amino acids as compared with normal controls. Similarly, treatment with alloxan was followed by decreased fasting levels of serum insulin, by increased fasting levels of blood glucose and plasma GIP, and by an increased GIP release in response to duodenal glucose and amino acids. The augmented GIP release in response to duodenal instillation of glucose and amino acids both in methylprednisolone-treated rats and in alloxan-treated rats may be explained by an increased absorption of these nutrients owing to an increased Na+ K+ ATPase activity in the intestinal mucosa of corticosteroid- and alloxan-treated rats. The elevated fasting GIP levels, on the other hand, are difficult to explain.

Alloxan↗
PubMed1982

Preparation of 125I-labeled gastric inhibitory polypeptide, using water-insoluble 1,2,4,6-tetrachloro-3 alpha,6 alpha-diphenylglycoluril (Iodo-gen) as the oxidizing agent.

The preparation and evaluation of a 125I-labeled gastric inhibitory polypeptide (GIP) by means of a modified Iodo-gen method are described. The portal vein fasting plasma GIP concentration was determined in 6 groups of rats with 10 rats in each group. In three of the groups, three separately prepared Iodo-gen tracers were used in the radioimmunoassay, and in the three other groups three separately prepared chloramine-T tracers were used. The mean fasting portal vein plasma GIP concentrations in the three groups were 45.0 +/- 5.0, 41.9 +/- 3.9, and 39.6 +/- 2.7 pmol/l, respectively, with the Iodo-gen tracers and 80.3 +/- 4.6, 78.4 +/- 5.4, and 85.7 +/- 3.7 pmol/l with the chloramine-T tracers. The values obtained in each of the groups with the Iodo-gen tracers were significantly lower than those obtained in each of the groups with the chloramine-T tracers. This may be due to a better preserved immunoreactivity of the Iodo-gen tracer than of the chloramine-T tracer. The explanation of this may be the water insolubility of Iodo-gen, which may prevent oxidation of easily oxidized residues of the peptide during the radioiodination procedure.

Animals↗
PubMed1982

The effect of atropine on plasma vasoactive intestinal polypeptide after intraduodenal infusion of fat in man.

Plasma vasoactive intestinal polypeptide (VIP) was measured in six healthy young men after intraduodenal infusion of 100 ml Lipomul (66 g triglycerides) on 2 separate days. On one of the days 0.5 mg atropine sulphate was injected intravenously at the start of the fat infusion, immediately followed by 0.75 mg atropine sulphate infused intravenously during the first hour. Plasma VIP rose significantly (p less than 0.05) and stayed significantly elevated for at least 120 min after intraduodenal infusion of fat alone. This effect was abolished by atropine, suggesting that the VIP release seen after intraduodenal fat may be dependent on a certain tone of muscarinic receptors influencing the VIPergic neurons. However, we cannot exclude the possibility that the blocking effect of atropine in part reflects a delayed transit time of fat in the intestine.

Adult↗
PubMed1982

Fasting portal vein plasma levels of gastric inhibitory polypeptide (GIP) and extractable fasting GIP in the duodenal wall in rats treated with methylprednisolone or alloxan compared with normal controls.

Ten rats were treated with methylprednisolone, another 10 rats with alloxan, and a final 10 control rats with saline. Compared with the controls, the methyl-prednisolone-treated rats had increased fasting levels of serum insulin, blood glucose, and plasma GIP; the alloxan-treated rats had decreased fasting levels of insulin and increased levels of fasting blood glucose and plasma GIP. After removal of the duodenum in the fasting state, the amount of GIP was measured in duodenal tissue specimens after extraction with ice-cold acetic acid, pH 3.0, and with neutralized acetic acid at 95 C. The duodenal content of GIP was 765.5 +/- 60.2 ng/g in the methylprednisolone-treated rats, 897.6 +/-37.3 ng/g in the alloxan-treated rats, and 923.1 +/- 72.9 ng/g in the saline-treated control rats. There were no significant differences in duodenal GIP content between the various groups, nor did the fasting plasma GIP and the amount of duodenal GIP in the individual rats correlate significantly (r=0.147, p less than 0.1). The elevated levels of fasting plasma GIP in the diabetic rats treated with methylprednisolone or alloxan may be due to factors regulating the secretion of GIP rather than to changes in the duodenal content of GIP.

Alloxan↗
PubMed1981

The response of plasma gastric-inhibitory polypeptide (GIP) to slow and fast glucose ingestion in Billroth II resected patients and normal controls.

Eight Billroth II resected patients and 8 normal controls were given two oral glucose loads, one ingested within 2 min, and the other ingested slowly over 80 min. In the Billroth II resected group, the integrated plasma GIP release was significantly higher after the fast than after the slow glucose ingestion. In this group the integrated plasma GIP release was also significantly higher than in the control group, but only after the fast glucose ingestion. These findings indicate that the rate of glucose delivery into the intestine may be of importance in the plasma GIP response to oral glucose.

Adult↗
PubMed1981

The effect of a test meal on plasma gastric inhibitory polypeptide and serum gastrin in patients with achlorhydria and hypergastrinemia, and in patients with normal gastric H+ secretion.

9 patients with achlorhydria and hypergastrinemia and 8 control patients with normal gastric H+ secretion and normal serum gastrin level were studied before and after a mixed liquid test meal. Mean plasma gastric inhibitory polypeptide increased to significantly higher values in the achlorhydric group than in the control group 30, 60 and 90 min after the meal. In the achlorhydric group mean serum gastrin fell significantly below the basal level 60 and 90 min after the meal, whereas a significant increase was observed in the control group.

Achlorhydria↗
PubMed1981

Gastric inhibitory polypeptide release into the portal vein in response to intraduodenal glucose loads in anesthetized rats.

Gastric inhibitory polypeptide (GIP) release into the portal vein in response to duodenal instillation of glucose in doses of 0.695, 1.39, 2.78 and 5.56 mmol/kg body weight was studied in an acute condition in male Wistar rats. A rapid, dose-dependent, and significant rise in portal vein plasma GIP was found in response to increasing duodenal glucose loads, which could be described by Michaelis-Menten kinetics. It is suggested that the glucose-induced GIP release into the portal vein mainly is effected first after glucose has gained access inside the mucosal cells.

Animals↗