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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Synthetic neurotensin was infused into five healthy subjects at a mean dose of 2.3 pmol/kg . min for 30 min, producing a rise in plasma neurotensin concentrations, measured by RIA of 104 +/- 10 (mean +/- SEM) pmol/liter. The mean disappearance half-time on stopping the infusion was 3.8 +/- 0.2 min. The MCR was 16 +/- 1 ml/kg . min, and the apparent space of distribution was 88 +/- 6 ml/kg. During the neurotensin infusions, plasma pancreatic polypeptide rose by 145 +/- 54 pmol/liter. In contrast to results in experimental animals, there was no significant change in the pulse or blood pressure of the subjects or any significant change in blood glucose or plasma concentrations of insulin, glucagon, gastric inhibitory peptide, gastrin, motilin, or vasoactive intestinal peptide. Similarly, there was no change in plasma concentrations of TSH, GH, PRL, LH, and FSH.
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PMID:Neurotensin infusion in man: pharmacokinetics and effect on gastrointestinal and pituitary hormones. 700 47

The effects of exogenous and endogenous hyperglycaemia on human pancreatic polypeptide secretion have been studied. In normal subjects elevation of plasma glucose concentration by glucose infusion both depressed the basal levels of circulating human pancreatic polypeptide (by 40-50%) and consistently reduced the human pancreatic polypeptide response to the ingestion of a portion-rich meal (areas above pre-meal value: 19.5 +/- 4.1 (mean +/- SEM) vs. 9.6 +/- 2.1, p < 0.01) as well as to caerulein infusion (areas above pre-caerulein value: 8.8 +/- 2.2 vs. 4.6 +/- 1.4, P < 0.01). In diabetic subjects treated with sulphonylureas or diet (fasting plasma glucose: 166 +/- 11 mg/dl, n = 24), human pancreatic polypeptide secretion evoked by food was similar to that of 24 healthy individuals (areas above basal value: 46.6 +/- 9.9 and 33.6 +/- 3.6, respectively). In insulin dependent diabetics (fasting plasma glucose: 231 +/- 19 mg/dl, n = 21) the human pancreatic polypeptide response to the meal (area above basal value: 78.2 +/- 13.7) was significantly greater than that of the controls as well as that of the noninsulin-dependent group (P < 0.05). Since the administration of pancreatic polypeptide to man has been shown to decrease pancreatic exocrine output, postprandial human pancreatic polypeptide hypersection may contribute to the decreased exocrin function of the pancreas often found in insulin-dependent diabetics.
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PMID:Human pancreatic polypeptide secretion in conditions of exogenous and endogenous hyperglycaemia. 700 59

The effect of the control of diabetes with diet and insulin upon plasma levels of human pancreatic polypeptide and glucagon was determined in eight patients with Type 2 (insulin independent) diabetes mellitus. The mean +/- SEM fasting plasma glucose was 15.9 +/- 1.3 mmol/l for 5 days of diet treatment and 5.9 +/- 0.4 mmol/l for the last 5 days of treatment with diet plus insulin (p less than 0.0001); corresponding fasting plasma pancreatic polypeptide levels were 328 +/- 97 and 247 +/- 71 pg/ml (p less than 0.05) and immunoreactive glucagon levels were 95 +/- 11 and 62 +/- 6 pg/ml (p less than 0.005). Cooked ground beef was administered on the first day of diet treatment and on the last day of treatment with diet plus insulin; mean maximal rise of pancreatic polypeptide, and total and incremental plasma pancreatic polypeptide response areas were significantly lower following treatment (p less than 0.01), as was total area for immunoreactive glucagon (p less than 0.05). Normalisation of fasting plasma glucose by short-term treatment with diet plus insulin is associated with decreases in basal and stimulated secretory activity of the pancreatic polypeptide cells in insulin independent diabetes mellitus.
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PMID:The effect of treatment of type 2 (insulin independent) diabetes mellitus on plasma concentrations of pancreatic polypeptide and glucagon. 702 Dec 84

1. Release of pancreatic polypeptide (PP) is largely under vagal control and measurement of change in PP after insulin hypoglycaemia offers a non-invasive method of assessing vagal activity. 2. Changes in blood sugar and PP after intravenous insulin (0.2 unit/kg) were examined in six patients with idiopathic chronic autonomic failure (AF) and 12 control subjects. Six of the controls were studied before and after atropine treatment. 3. The PP levels in controls rose from 32 +/- 9 (mean +/- SEM) to 236 +/- 54 pmol/l after 45 min. Patients had similar baseline values (23 +/- 5 pmol/l) but a markedly reduced and delayed PP response to hypoglycaemia (49 +/- 19 pmol/l at 90 min). This impaired PP response was similar to that seen in controls after atropine. 4. The impaired PP response to insulin hypoglycaemia in patients with AF strongly suggests a dysfunction of vagal activity which is often clinically inapparent.
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PMID:Impaired pancreatic polypeptide release to insulin hypoglycaemia in chronic autonomic failure with postural hypotension: evidence for parasympathetic dysfunction. 704 53

To assess the possible value of the use of high-purity pork insulin (HPPI) in the United States, the serum insulin (I), pancreatic polypeptide (PP), glucagon (G), and somatostatin (SRIF) antibody binding characteristics have been determined in 90 conventional insulin-treated diabetic subjects and related to their degree of metabolic control, as assessed by glycosylated hemoglobin (HbA1) concentration. All diabetic subjects had antibodies to insulin, but there was no relationship between any of the antibody binding characteristics and HbA1 level: 47% possessed PP antibodies; mean +/- SEM HbA1 in these patients was 14.5 +/- 0.3%, identical to those without PP antibodies (14.5 +/- 0.4%); 10% had G binding antibodies with HbA1 levels of 14.6 +/- 0.8%, similar to those without G antibodies. No subject possessed SRIF antibodies. This lack of correlation between antibody characteristics and metabolic control makes it unlikely that, in the majority of patients, treatment with a less immunogenic insulin (HPPI) versus conventional insulin will result in improved diabetic control.
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PMID:Insulin, pancreatic polypeptide, and glucagon antibodies in insulin-dependent diabetes mellitus. 704 10

Hypoacidity and hypergastrinaemia are reported in the newborn human. To investigate the ontogeny of gastrin, plasma gastrin concentrations were measured in chronically cannulated foetal sheep from 100 days gestation to term (145 days) and up to 16 days following delivery. Plasma pancreatic polypeptide (PP) concentrations were measured as a marker of vagal activity. Compared with adult values, foetal plasma gastrin concentration was low at 101-105 days, being 7 +/- 1 pmol/l (mean +/= SEM) but greater than adult values from 130 days gestation and increased to 47 +/- 5 at 141-145 days, and 90 +/- 13 at 1-5 days post-partum. Maternal plasma gastrin level during these periods ranged between 21 and 29 pmol/l and was not related to gestational age. Similarly, maternal plasma PP levels, which varied between 220 and 400 pmol/l, did not correlate with gestational age and did not differ significantly from non-pregnant sheep. Foetal plasma PP was low, 20 +/- at 101-105 days, rose to 92 +/- 17 at 141-145 days, and increased to adult levels in the first week post-partum. Basal foetal and maternal plasma PP were inhibited by iv atropine injection. The increase in plasma PP may represent a maturity of vagal influence. Gastrin and PP have a trophic action on the gastro-intestinal tract, so the observation of significant levels of circulating gastrin and PP in the foetus suggests that they may be involved in maturation of the gastro-intestinal tract.
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PMID:Ontogeny of circulating gastrin and pancreatic polypeptide in the foetal sheep. 712 79

Pancreatic polypeptide (PP) can be used as a marker for endocrine active tumors originating from the pancreas. After intravenous administration of secretin, individually divergent increases in plasma PP concentration can be observed hampering interpretation of the stimulation test. Under certain circumstances elevated basal PP concentrations can be observed. Besides age, renal insufficiency and diabetes, hypoglycemia can cause high PP levels. We therefore inquired whether in patients with atypically high increase of PP after secretin this increase could be caused by hypoglycemia during the secretin stimulation test. In order to test this hypothesis we prospectively determined the plasma glucose and insulin concentrations in addition to the routinely measured gastro-intestinal hormones in 19 patients referred for secretin provocation test. In the 16 patients in whom the increase of PP was not due to an endocrine active tumor or renal insufficiency, PP rose to 170 +/- 57 pmol/l (+/- SEM) 2 minutes after secretin administration. In parallel, plasma insulin concentration increased to 365 +/- 51 pmol/l 2 minutes after secretin. The maximal insulin concentrations correlated significantly with the PP concentrations observed at the same time (R = 0.73, p < 0.01). The mean glucose concentration, however, remained constantly between 4.8 +/- 0.3 and 5.2 +/- 0.3 mmol/l and there was no correlation between the peak plasma PP concentrations after secretin and the plasma glucose concentrations (R = 0.07). The minimal glucose concentrations observed were 3.3 mmol/l in three patients (30 minutes after secretin in 2 patients and 45 minutes after secretin in one). The mean plasma glucagon concentration rose to 22.5 +/- 4.1 pmol/l 10 minutes after secretin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Abnormal increase in pancreatic polypeptide in the secretin-provocation test: hypoglycemia-induced?]. 774 Feb 87

Pancreatic graft procurement, preservation, and transplantation surgery may result in damage to and loss of the integrity of endocrine cells and consequently in leakage of cell products into the insular vascular capillaries. Thus, the amount of alpha-, beta-, and pancreatic polypeptide (PP) cell products released into the vascular space of the recipient immediately after graft reperfusion may reflect islet cell injury. To test this hypothesis, we assessed glucagon, PP, C-peptide, and insulin levels in a prospective study of 22 consecutive renal-pancreatic transplantations. Transplantation-related parameters were used to account for differences in hormone release. Five grafts were preserved using Euro-Collins preservation fluid and 17 grafts were preserved using University of Wisconsin solution (UW). The first sign of a reinstalled physiological axis was the decrease of the blood glucose concentration after a median duration of 40 min (range 5-90 min) and the association of the recipient's ambient blood glucose levels with insulin release between 25 and 180 min after reperfusion. The delay period before a fall in blood glucose was observed correlated with cold ischemia time (rs = 0.73, P < 0.001, n = 21). An immediate and marked increase in plasma levels of glucagon (from 180 +/- 18 to 585 +/- 99 ng/L, mean +/- SEM), PP (from 57 +/- 8 to 122 +/- 13 pmol/L), C-peptide (from < 0.06 +/- 0.02 to 5.43 +/- 0.63 nmol/L), and insulin (from 0.15 +/- 0.21 to 2.05 +/- 0.26 nmol/L) was observed. C-peptide release correlated with glucagon (r = 0.76, P < 0.001) and PP (r = 0.60, P < 0.01). The hormone release was compared with computed tomography scans that were performed in the immediate postoperative period in 15 UW-preserved allografts. The diameter of the pancreatic head was increased and ranged from 4.5 to 7.7 cm (mean 6.2 cm). Peroperative C-peptide release significantly correlated with morphological graft changes reflected by the pancreatic head diameter (r = 0.58, P = 0.02). In a stepwise multiple regression analysis, cold ischemia time was a significant factor for the release of PP (r2 = 0.18, P = 0.049) and C-peptide (r2 = 0.35, P = 0.004). We suggest that peroperative hormone release reflects endocrine tissue damage. Furthermore, cold ischemia time may jeopardize the pancreatic allograft after relatively short preservation times, even when UW is used.
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PMID:Islet cell hormone release immediately after human pancreatic transplantation. A marker of tissue damage associated with cold ischemia. 824 11

The neuropeptide galanin (GAL) is widely distributed in the central and peripheral nervous systems where it often coexists with catecholamines and acetylcholine. Recently we have reported that human GAL (hGAL) in man depresses the release of norepinephrine (NE) and the responses to both assumption of upright posture and insulin-induced hypoglycemia. To gain an insight into the action of hGAL on sympathetic nervous system activity in man, we investigated the effects of a 60-min infusion (80 pmol/kg/min) of hGAL or saline on the release of NE, epinephrine (E) and pancreatic polypeptide (PP) induced by an acetylcholinesterase inhibitor, pyridostigmine bromide (PD), in nine healthy volunteers. PD (120 mg orally) induced a significant rise in plasma concentrations of NE (1.6 +/- 0.04 vs. 1.08 +/- 0.06 nmol/l), E (0.34 +/ 0.05 vs. 0.12 +/- 0.04 nmol/l) and PP (178.06 +/- 33 vs. 37.57 +/- 7.35 pmol/l), whilst it significantly reduced heart rate (HR; 61 +/- 2 vs. 71 +/- 4 beats/min). Changes in plasma levels of PP were determined as an indirect measure of amplification of endogenous cholinergic activity produced by PD. Administration of hGAL blunted the release of NE and PP evoked by PD. The mean (+/- SEM) area under the curve produced by PD of NE (50.05 +/- 3.97 nmol/l.90 min) and PP (8,692.87 +/- 1,724 pmol/l.90 min) was significantly (p < 0.001) reduced by hGAL infusion (2.65 +/- 1.57 nmol/l.90 min and 248.1 +/- 148 pmol/l.90 min, for NE and PP, respectively). hGAL failed to affect significantly the E release evoked by PD. hGAL was able to enhance HR significantly (104 +/- 5 vs. 69 +/- 3 beats/min), and completely prevented the PD-induced slowing of HR. Both PD and hGAL did not alter supine systolic and diastolic blood pressure. We conclude that hGAL significantly reduces the release of NE and PP stimulated by PD-induced enhancement of cholinergic activity. These findings are consistent with a functional interrelationship between GAL and the cholinergic system in man, and may suggest the participation of a cholinergic pathway in the galaninergic modulation of the autonomic nervous system.
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PMID:Acute administration of human galanin in normal subjects reduces the potentiating effect of pyridostigmine-induced cholinergic enhancement on release of norepinephrine and pancreatic polypeptide. 893 Sep 40

To establish whether the incretin effect is under neural control, insulin, C-peptide, and glucose-dependent insulinotropic peptide (GIP) responses and hepatic insulin clearance were investigated after oral and "isoglycemic" intravenous glucose in 12 inbred rats after denervation of the pancreas by orthotopic transplantation with portal venous drainage (Tx group) and in 12 laparotomized controls (sham group). Effective pancreas denervation was documented by a decreased pancreatic polypeptide (PP) response to insulin-induced hypoglycemia and by decreased levels of norepinephrine and calcitonin gene-related peptide (CGRP) in pancreatic tissue. Basal and incremental arterial plasma glucose integrated over 180 minutes did not differ between oral and intravenous glucose, but the integrated insulin response (mean +/- SEM) was significantly greater with oral versus intravenous glucose (Tx group, 104.9 +/- 22.0 v 31.0 +/- 4.9 nmol x L(-1) x min, P < .01; sham group, 79.5 +/- 10.6 v 36.6 +/- 5.8 nmol x L(-1) x min, P < .01). The integrated response of C-peptide was similar during both tests (Tx group, 105 +/- 14 v 79 +/- 8 pmol x mL(-1) x min; sham group, 112 +/- 10 v 121 +/- 12 pmol x mL(-1) x min). Hepatic insulin clearance was significantly decreased in both groups by oral compared with intravenous glucose administration (Tx group, 1.3 +/- 0.2 v 3.3 +/- 0.6 mmol/mmol, P < .01; sham group, 1.6 +/- 0.1 v 3.9 +/- 0.6 mmol/mmol, P < .02). The incretin effects for insulin (Tx group, 5.6 +/- 2.7; sham group, 3.0 +/- 0.8) and C-peptide (Tx group, 1.4 +/- 0.2; sham group, 1.1 +/- 0.2), calculated as the ratio of the integrated oral response and integrated intravenous response, and GIP responses to oral and intravenous glucose were not significantly different between the two groups. We conclude that there is preservation of the incretin effect in rats with orthotopically transplanted and hence extrinsically denervated pancreas, thus ruling out the possibility that the autonomic nervous system substantially contributes. Hepatic insulin clearance and insulinotropic hormones such as GIP appear to be more important.
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PMID:Preservation of the incretin effect after orthotopic pancreas transplantation in inbred rats. 1033 68


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