Gastrointestinal insulinotropic hormones in normal and gestational-diabetic pregnancy: response to oral glucose.

The responses of gastric inhibitory polypeptides (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, and pancreatic glucagon to a 50-g oral glucose load were studied in late pregnancy and postpartum in 11 normal women, 10 normal weight gestational diabetics, and 10 overweight gestational diabetics. The GIP response to glucose was impaired in pregnancy in all three groups. In pregnancy, the GIP response was smaller in both groups of gestational diabetics than in normal women, whereas postpartum, the GIP response was lower than normal in the normal weight gestational diabetics only. In pregnancy, the gut GLI response to glucose was reduced in the overweight gestational diabetics and abolished in the normal women. The insulin response to glucose was increased in pregnancy in all three groups. Moreover, it was higher in the overweight gestational diabetics than in the other two groups in pregnancy and postpartum. In the normals, the suppression of glucagon levels after glucose ingestion was more marked in pregnancy than postpartum, whereas no such effect was seen in gestational-diabetic pregnancy. It is concluded that pregnancy--normal as well as gestational-diabetic--is accompanied by profound changes in the secretion of gastrointestinal insulinotropic hormones after glucose ingestion. These findings may be important for the understanding of changes in metabolism and gastrointestinal physiology in gestation.

Gastric inhibitory polypeptide and insulin: response to intraduodenal and intravenous glucose infusions in fetal and neonatal pigs.

The responses of gastric inhibitory polypeptide (GIP) and insulin to intraduodenal (OGTT) and iv (IVGI) glucose infusions were measured in 14 late fetal and 9 neonatal pigs. Basal plasma glucose (P < 0.01) and GIP (P < 0.001) concentrations were lower in the fetal than in the neonatal pigs, while basal plasma insulin was not significantly different in the two groups. In the fetal pigs, almost identical plasma glucose curves were obtained during the OGTT and the IVGI, but plasma insulin did not change during either test. In these pigs, plasma GIP increased 3-fold (P < 0.01) during the OGTT, whereas no significant changes in plasma GIP were observed during the IVGI. In the neonatal pigs, plasma glucose increased more during the OGTT than during the IVGI, but plasma insulin exhibited similar increments during both tests. Thus, the insulinogenic index of the IVGI was almost 3 times higher than that of the OGTT (P < 0.05). In contrast to the normal increment in plasma GIP observed in fetal pigs, plasma GIP decreased significantly during both tests in the neonatal pigs. It is concluded that beta-cells of fetal pigs are unresponsive to acute elevations of plasma glucose with or without a concomitant increase in plasma GIP. Conversely, beta-cells of neonatal pigs exhibit a significant response to hyperglycemia, but the enteroinsular axis is defective, since more insulin is released after iv than during intraduodenal glucose administration. The defective enteroinsular axis in neonatal pigs might be due to the observed fall in plasma GIP during the OGTT.

Diminished gastric inhibitory polypeptide response to oral glucose in late human pregnancy.

It has been shown that the incretin effect - i.e. the gastrointestinal potentiation of the insulin response to oral glucose - is reduced in late normal pregnancy. As evidence points to gastric inhibitory polypeptide (GIP) as mediator of at least part of the incretin effect, the GIP response was determined following a 50 g oral glucose load in 6 normal women in the last trimester of pregnancy and again post partum. Compared to post partum the GIP response to oral glucose was significantly impaired in late pregnancy. It is concluded that the diminished GIP response to oral glucose in late pregnancy might at least partly explain the impaired incretin effect found in this condition.

Gastric inhibitory polypeptide (GIP) and insulin release in response to oral and intravenous glucose in uremic patients.

Eight patients with advanced renal failure of long duration were studied 1 day after hemodialysis. A 50 g oral glucose load (OGTT) and an intravenous glucose infusion (IVGI), giving the same plasma glucose profile as the OGTT, were carried our in order to study the relation between Gastric Inhibitory Polypeptide (GIP) plasma levels after oral glucose and the insulin release during OGTT and IVGI. The plasma GIP increase during OGTT was significantly elevated compared to a group of eight healthy volunteers. The insulin potentiation during OGTT in relation to GIP was significantly depressed in the uremic patients. It is proposed that a factor of intestinal origin is released during intake of carbohydrates, which blocks the B-cell response to the combined glucose-GIP stimulus. Alternatively, the concentrations of plasma GIp measured have included GIp fragments without insulin releasing capability.

Simultaneous recording of the gastro-entero-pancreatic hormonal peptide response to food in man.

The serum or plasma concentrations of gastrin, gastric inhibitory polypeptide (GIP), gut glucagon-like-immunoreactivity (gut GLI), secretin, vasoactive intestinal polypeptide (VIP), insulin, glucagon, and pancreatic polypeptide (PP) were recorded simultaneously following the ingestion of a normal, mixed meal in seven healthy, normal weight men. The concentrations of PP and gastrin increased within 10 min. Subsequently GIP, insulin, glucagon, and gut GLI increased in the order mentioned. The mean concentrations of secretin and VIP were not affected by the meal, athough transient decreases in secretion concentrations could be detected in all subjects. The concentrations of the other hormones remained elevated for 4 hr or more. Perhaps the period of observation following food stimulation of gastro-entero-pancreatic hormones should be extended.

Mesenchymal tumor hypoglycemia: the effect of a tumor tissue extract on the insulin and glucagon secretion from the isolated perfused porcine pancreas.

Severe fasting hypoglycemia and hypoinsulinemia occurred in a sixty-six year old woman with an intrahepatic mesenchymal tumor. An extract from the tumor was potent in inhibiting the arginine-induced glucagon secretion from the isolated perfused porcine pancreas. This observation supports the theory recently advanced that mesenchymal tumor hypoglycemia in some cases is due to a still unknown factor secreted from the tumor, which directly inhibits pancreatic glucagon secretion.

Basal hyposecretion of gastric inhibitory polypeptide after Roux-Y hepaticojejunostomy in man.

We previously showed that basal and pentagastrin-stimulated gastric acid secretion, gastrin in serum and gastrin in antral mucosa were significantly greater in patients with Roux-Y hepaticojejunostomy than in those with choledochoduodenostomy. These findings prompted investigation of basal secretion of gastric inhibitory polypeptide (a peptide with an enterogastrone as well as an insulinogenic effect), insulin and glucose in the same patients. Basal gastric inhibitory polypeptide was significantly lower in patients with Roux-Y hepaticojejunostomy than in those with choledochoduodensotomy, whereas glucose and insulin did not differ in the two groups. No correlation could be demonstrated between gastric inhibitory polypeptide, gastric acid secretion and gastrin, suggesting that hyposecretion of gastric inhibitory polypeptide is not a pathogenetic factor for the hypersecretion of gastric acid secretion in patients with Roux-Y hepaticojejunostomy. Hyposecretion of gastric inhibitory polypeptide and gastric acid hypersecretion in patients with bile diversion seem to be two independent phenomena.

[Erosion of the splenic artery in acute pancreatitis]. / Arteria lienalis arrosion ved akut pancreatitis.

A patient with bleeding from the eroded distal splenic artery secondary to acute pancreatitis is presented. The pancreatic tail was found to be moderately edematous without cyst, abscess or necrosis at splenectomy. The walls of the artery showed no structural changes. The postoperative course was uneventful.

[The palliative effect of bilateral orchiectomy in metastatic cancer of the prostate]. / Den palliative effekt af bilateral orkiektomi ved metastaserende prostatacancer.

The effect of bilateral orchidectomy in relieving pain in 70 patients with metastatic carcinoma of the prostate was investigated by review of the case reports of a patient material from a urological department. 74% of the patients stated that the intervention was effective. Relief of pain lasting for more than seven months and attributable solely to the orchidectomy occurred in 19%. It did not prove possible to differentiate by means of biochemical or clinical parameters between the patient groups with and without beneficial effects from the intervention. 30% died during the first postoperative year. The five year survival rate was calculated to be 19%.

Insulin secretion in the Zollinger-Ellison syndrome.

The insulin response to oral glucose ingestion was measured in six patients with the Zollinger-Ellison (ZE) syndrome, five patients with partial gastrectomy (antrectomy for duodenal ulcer) and six matched normal subjects. The blood glucose curves were similar in ZE-patients and gastrectomized controls and significantly above the glucose concentrations in normal controls. The insulin response was three-doubled in ZE-patients, whereas gastrectomized controls only doubled their response in comparison with the normal subjects. Treatment of a hepatic gastrinoma by streptozotocin infusion into the hepatic artery in a patient with diabetes mellitus and hyperinsulinism almost normalized his glucose tolerance and insulin secretion. The results demonstrate that the ZE-syndrome is associated with increased insulin release. We suggest that the hyperinsulinism partly is a consequence of previous gastric surgery and partly due to the insulinogenic effect of gastrin.

Serum-gastrin in cirrhosis.

Fifty patients with cirrhosis of the liver had gastrin concentrations in serum above normal when measured in the fasting state. Hypergastrinaemia predominated in non-alcoholic cirrhosis. In both groups of patients, serum gastrin levels were higher in patients with inactive cirrhosis than when cirrhosis was slightly active.