Serum Concentrations Of Pancreatic Polypeptide Research Articles

Screening For Multiple Endocrine Neoplasia Type 1 In Patients With Recognized Pituitary Adenoma

A total of 79 consecutive patients with pituitary tumours were screened for multiple endocrine neoplasia type 1 (MEN-1). The 79 patients included 21 patients with acromegaly, nine with Cushing's disease, 18 with prolactinomas, three with mixed pituitary adenomas (GH and PRL), and 28 patients with no detectable hypersecretion of hormones. The screening consisted of: (1) a family history, (2) a uniform medical history of the patient using a standard questionnaire, and (3) hormonal evaluation including measurements of the serum levels of insulin, gastrin, glucagon, somatostatin, vasoactive intestinal polypeptide and pancreatic polypeptide. Ionized calcium and glucose concentration in serum were also measured. We found no patients with the MEN-1 syndrome. In one patient, we found a transient elevation of serum concentrations of pancreatic polypeptide for which we have no explanation. In another patient, the serum gastrin concentration was elevated secondary to achlorhydria. No other endocrine disorders were found, and no patients had relatives with recognized endocrine pancreatic tumours, primary hyperparathyroidism (HPT), or pituitary adenomas.

Increased serum pancreatic polypeptide and serum gastrin secretion in patients with functional dyspepsia: correlation to the shape of the duodenal loop

Simultaneous measurement of food-stimulated serum pancreatic polypeptide and serum gastrin was carried out in 18 patients with functional dyspepsia and correlated to the shape of the duodenal loop. Significantly higher serum concentrations of pancreatic polypeptide and gastrin were encountered in patients with an abnormal shape of the duodenal loop compared to patients with a normal shape. Although no cause could be given to the phenomenon it may be taken into account when evaluating hormone profiles in patients with functional dyspepsia.

Serum concentration of pancreatic polypeptide in normal subjects and in peptic ulcer patients.

The present study evaluates the serum concentration of pancreatic polypeptide (PP) in normal male and female subjects of different ages (ranging from 20 to 69) and also in patients with peptic ulcers. The PP level rose with age and was higher in the male subjects (from the age of 30). Serum levels of the peptide in patients with gastric or duodenal ulcers were not significantly different from the normal subjects (age and sex matched with the diseased groups).

Mechanism of elevated serum pancreatic polypeptide concentrations in chronic renal failure.

Basal serum concentrations of pancreatic polypeptide (PP) in five patients with chronic renal failure (CRF; 165-2100 pmol/liter) were significantly (P less than 0.01) higher than those in six age-matched normal control subjects (18-54 pmol/liter). Ingestion of a mixed meal resulted in significantly (P less than 0.01) larger increases in serum PP in patients with CRF (245-1740 pmol/liter) than in the normal subjects (72-196 pmol/liter). The iv administration of somatostatin (125 micrograms as a bolus injection, followed by infusion of 125 micrograms/h) to two patients with CRF and two normal subjects completely abolished postprandial PP release. By administering the same dose of somatostatin 60 min after ingestion of the meal, the disappearance rate of endogenously released PP could be estimated. The half-life of disappearance for PP in patients with CRF (t1/2 = 13.2 +/- 1.8 min) was significantly (P less than 0.01) increased compared to that in the normal subjects (t1/2 = 5.6 +/- 0.8 min). Sephadex G-50 column chromatography of basal sera from three patients with CRF revealed three major peaks of PP: one eluting in the void volume, one coeluting with the 4200 molecular weight human PP standard, and one in between. The PP peak coeluting with standard PP comprised 64 +/- 3% of total PP immunoreactivity. Ingestion of food, followed by subsequent infusion of somatostatin, resulted in marked changes in the PP peak coeluting with standard PP, while the two larger molecular forms remained relatively unchanged. At least three findings may be related to the mechanism of elevated serum PP concentrations in patients with CRF: 1) the presence of large molecular forms of PP, 2) a slower disappearance rate for postprandially released PP, and 3) increased postprandial secretion of PP indicating hyperresponsiveness of PP cells to physiological stimuli.

Dose-dependent increase in concentrations of gastric inhibitory polypeptide and pancreatic polypeptide after small amounts of glucose intraduodenally in man.

Nine healthy volunteers were infused intraduodenally with 100 ml isotonic solutions of 1, 2.5, and 5 g glucose for 15 min at 1-h intervals. The gastric inhibitory polypeptide (GIP) concentration in plasma did not increase after 1 g of glucose, whereas after 2.5 g of glucose the GIP concentration increased from 32.1 (23.3-68.4) to 53.9 (30.0-63.0) pM and after 5 g from 36.8 (18.0-54.7) to 78.5 (46.9-163) pM. The serum concentration of pancreatic polypeptide (PP) increased only after 5 g, from 19.3 (14.8-29.1) to 28.8 (15.3-45.3) pM. This shows that the plasma concentration of GIP increases dose-dependently after small doses of duodenal glucose and that glucose really is a duodenal stimulus for an increase i serum PP concentration.

Dose-response study of somatostatin on meal-stimulated levels of pancreatic polypeptide and insulin in the dog.

A dose-response study of the effect of 0.1-5.0 micrograms kg-1 h-1 somatostatin was performed on food-induced rise of pancreatic polypeptide and insulin in 4 dogs. There was a dose-dependent suppression of the release of pancreatic polypeptide and insulin with an ED50 of approximately 0.65 and 0.8 microgram kg-1 h-1, respectively, during the first 45-min period. In the second 45-min period, high doses of somatostatin failed to suppress insulin concentrations whereas, the serum concentrations of pancreatic polypeptide were reduced by a similar degree as in the first 45 min. The differing effects of somatostatin on food-stimulated serum concentrations of insulin and pancreatic polypeptide indicate that somatostatin does not represent a uniform suppressor of pancreatic hormones.

Serum concentration of pancreatic polypeptide after infusion of histamine and the effect of cimetidine, trimipramine, and atropine in man.

Histamine was given intravenously to eight human subjects, and the PP concentration in serum increased significantly from 14.8 (7.2-29.3) pM to 27.5 (9.6-39.3) pM and then decreased to the basal level. This histamine-induced PP release was not altered when trimipramine or cimetidine was given in addition to histamine. This PP release could not mediated through histamine-receptor mechanisms, and since atropine prevented this PP release, we conclude that the release of PP after histamine reflects a cholinergic stimulus.

Basal and postprandial serum concentrations of pancreatic polypeptide in pancreatitis and after pancreaticoduodenectomy.

Summary Basal and postprandial serum concentrations of pancreatic polypeptide (PP) were measured in 22 normal subjects, in 6 patients with a history of acute pancreatitis, in 21 patients with chronic pancreatitis and in 6 patients with previous pancreaticoduodenectomy. Eighteen of the 21 with chronic pancreatitis and all 6 with pancreaticoduodenectomy had abnormally low serum PP-responses to the standard test meal, while all patients with a history of acute pancreatitis had normal postprandial increases in serum PP. The impaired serum PP-responses to food in patients with chronic pancreatitis were not related to the aetiology of pancreatitis, to glucose tolerance, to exocrine pancreatic function (absorption of fat) or to pancreatic calcifications. It is concluded that impaired postprandial serum PP responses in patients with pancreatitis indicate damage to the pancreas.

Gastric acid secretion in uraemia and circulating levels of gastrin, somatostatin, and pancreatic polypeptide.

Basal circulating levels of gastrin, somatostatin, and pancreatic polypeptide were measured in 30 chronic haemodialysis patients. Five patients had considerably raised serum gastrin (greater than 400 pmol/1) and also gastric achlorhydria while 75% of the patients who had normal (less than 55 pmol/1) or moderately increased (less than 400 pmol/1) serum gastrin had raised maximal acid outputs. Patients with serum gastrin greater than 400 pmol/1 had significantly lower plasma concentrations of somatostatin compared with both healthy individuals and uaremic patients with normal gastrin levels. Raised serum concentrations of pancreatic polypeptide were observed in the majority of the patients but no correlation was found between this peptide and gastric acid secretion or circulating levels of gastrin and somatostatin, respectively. Prolonged circulation time for gastrin and pancreatic polypeptide was demonstrated after food stimulation. Prolonged gastrin stimulation of the parietal cell mass may lead to work hypertrophy and gastric acid hypersecretion. Whether long-standing over-stimulation by gastrin also may induce atrophy of the cells remains to be studied.