Biomedical subjects
Publications and source records attributed to R Jorde.
Insulin-induced hypoglycemia caused a modest but significant (p = 0.031) increase in plasma GIP. This increase was significantly (p = 0.031) attenuated when atropine was given together with insulin, indicating that the vagal nerves play a major role in the release of plasma GIP during hypoglycemia.
Five morbidly obese patients were studied with a liquid test meal before and 2 and 6 weeks after jejunoileal bypass. Before the operation the postprandial GIP release was similar to that seen in a group of eight normal control subjects, whereas after surgery the postprandial GIP release was almost abolished. On the other hand, in a group of eight patients operated on identically more than 2 years ago, mean plasma GIP increased significantly after the meal, reaching values half those seen in the control group. This indicates that compensatory changes, affecting the plasma GIP release, occur in th remaining functioning intestine. As compared with the preoperative values, the meal-induced rise in mean serum insulin was significantly reduced 2 and 6 weeks after the bypass operation, together with a flattening of the postprandial blood glucose curve. The postprandial serum insulin and blood glucose values seen in the group operated on more than 2 years ago were similar to those seen in the group studied shortly after the operation.
Six healthy men were studied with a 10-min intraduodenal infusion of 100 ml corn oil (66 g triglycerides) on 2 separate days. On one of the days 0.5 mg atropine sulfate was also given intravenously before start of the fat infusion, followed by 0.75 mg atropine sulfate infused during the first hour. On the day without atropine, plasma GIP and serum insulin increased significantly. The increases in plasma GIP and serum insulin were significantly attenuated by atropine. Blood glucose fell on both days, the fall being slightly delayed by atropine.
In a group of 10 patients undergoing routine cardiac catheterization, mean plasma gastric inhibitory polypeptide (GIP) was significantly lower (p = 0.002) in blood drawn from the renal vein than in blood drawn from the hepatic vein, the right atrium, the femoral vein, and the femoral artery, demonstrating the removal of immunoreactive GIP by the kidneys. In a group of eight nephrectomized rats, mean plasma GIP was significantly higher 30 and 60 min after start of intraduodenal glucose infusion (p = 0.03 and p = 0.002, respectively) as compared with eight control rats, which probably reflects reduced removal of GIP in the nephrectomized group.
Duodenal juice was collected before and after an intragastric infusion of 300 ml 25% glucose in five healthy subjects. After extraction with 95% ethanol, IR-GIP in duodenal juice was determined by radioimmunoassay and found to increase from mean basal level of 63 pmol/l to a mean peak of 354 pmol/l after the glucose infusion. The elution diagrams of IR-GIP in glucose-stimulated duodenal juice and the corresponding plasma from a 16 X 400 mm Sephadex G-50 Fine column were similar, and the radioimmunoassay dilution curves of porcine GIP and duodenal juice IR-GIP were superimposable.
Six healthy men were given a standard breakfast, one day with and another day without a 2-h 100 micrograms/h somatostatin infusion. During the somatostatin infusion the meal-induced responses of plasma GIP and serum insulin were completely blocked, whereas the rise in blood glucose was significantly augmented. After termination of the somatostatin infusion the mean plasma GIP increased gradually to a peak after 2 h, whereas mean serum insulin showed a marked rebound phenomenon and peaked after 30 min, on the one hand, and mean blood glucose fell to an apparent nadir after another 30 min, on the other. The effect of somatostatin on basal plasma GIP, serum insulin, blood glucose, and gastric H+ secretion was studied in another group of six healthy men. Mean plasma GIP tended to fall during the initial 1-h saline infusion, fell further during the first part of the 2-h 100 micrograms/h somatostatin infusion, and started to rise first 85 min after termination of the somatostatin infusion. Similarly, mean serum insulin, mean blood glucose, and mean gastric H+ secretion decreased during the somatostatin infusion, and thereafter returned to their basal levels.
The meal-induced rises in plasma GIP, serum insulin, and blood glucose were studied after an overnight fast and after a 34-h fast in six healthy men. After the 34-h fast, the postprandial mean plasma GIP level at 120 min and the mean serum insulin and blood glucose levels at 60 and 90 min were significantly higher than those seen after the overnight fast.
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A sensitive, precise and specific radioimmunoassay method for measuring plasma gastric inhibitory polypeptide (GIP) is described. The present assay system, using a label purified on a Sephadex G-15 and a SP Sephadex C-25 column as well as careful corrections for nonspecific plasma effects, allows measurements of fasting plasma GIP in the lower picomole per liter range, and the significant rise in plasma GIP subsequent to a test meal and duodenal infusion of cattle bile. Apparent immunoreactive fasting plasma GIP was eluted from a Sephadex G-150 Fine column in one peak probably representing plasma GIP bound to plasma proteins and nonspecific plasma effects. Apparent immunoreactive meal-stimulated plasma GIP was eluted from a Sephadex G-50 Fine column in two large and one diminutive peak. The first peak probably represents plasma GIP bound to plasma proteins and nonspecific plasma effects, the almost negligible second peak probably represents big GIP with a molecular weight of some 9,000, and the third and major peak, little GIP with a molecular weight of about 5,000.
Thirteen persons with normal pentagastrin-stimulated gastric H+ secretion and 17 with achlorhydria were studied with a liquid test meal after an overnight fast. Blood was drawn before and every 30 min for 180 min after start of the meal. Serum gastrin, serum PG I, and serum vitamin B12 were determined by radioassay methods. Serum PG I was significantly lower in the achlorhydric subjects than in the normal secretors. The meal induced a slight and late rise in serum PG I in the control group. In contrast, the meal caused a slight fall in the achlorhydric persons. Basal serum gastrin was significantly higher in the achlorhydric group, in whom the meal also caused a significant fall in serum gastrin, which contrasts sharply with the rise in the control group. Although serum gastrin fell significantly in the achlorhydric group, a meal-induced rise in serum gastrin was observed in some of the achlorhydric subjects with basal serum gastrin below 100 pmol/l. Serum vitamin B12 was reduced in 8 of the 17 persons with achlorhydria, and in these 8 subjects serum PG I was significantly lower than in those with achlorhydria and normal serum vitamin B12.
Nine healthy young male students were studied before, during, and after a 10-min period of duodenal infusion of 6 g dried cattle bile dissolved in 75 ml distilled water to iso-osmolarity and pH adjusted to pH 7.0. Plasma vasoactive intestinal polypeptide (VIP), gastric inhibitory polypeptide (GIP), and duodenal bicarbonate secretion increased significantly, whereas plasma secretin showed a late but not significant tendency to rise after the bile infusion.
Plasma gastric inhibitory polypeptide (GIP) was studied for 24 h in six healthy, young men who ate four meals and performed their usual physical activities. Plasma GIP peaked after each meal and stayed significantly elevated from the peak after breakfast till late evening.
A precise and specific radioimmunoassay method for measuring plasma cholecystokinin (CCK) is described. The present assay system using a stable tracer iodinated by means of a modified Chloramine-T method followed by purification on a Sephadex G-15 and a SP Sephadex C-25 column, as well as careful corrections for non-specific plasma effects, allows measurements of fasting plasma CCK in the low pmol/l range; the significant rise in plasma CCK following duodenal infusion of fat; and the significant diurnal variation of plasma CCK. Apparent immunoreactive meal-stimulated plasma CCK was eluted from a Sephadex G-50 superfine column in four fractions. The first and largest peak probably represents plasma CCK bound to plasma proteins and non-specific plasma effects, the second and smaller peak big CCK with molecular weight between some 5,000 and some 30,000, the shoulders following the second peak ordinary CCK33 and CCK39 variant, and the final, and by far the smallest peak, may possibly represent COOH-terminal tetra- (CCK4) or octapeptides (CCK8) of CCK.
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In six fasting healthy young male students a 15-min test meal consisting of 160 ml milk, 200 ml coffee, 70 g bread, 3.5 g butter, 35 g cheese, and 30 g ham (45 g carbohydrates, 30 g proteins, and 25 g fat) caused a late but significant elevation in plasma vasoactive intestinal polypeptide (VIP), an early and sustained significant rise in plasma gastric inhibitory polypeptide (GIP), but no significant change in plasma secretin.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.