Search PubMed⌕ Search

Biomedical subjects

T E Adrian

Publications and source records attributed to T E Adrian.

At least 289 records · Page 16Linked to original sources

Breast vs bottle: endocrine responses are different with formula feeding.

Differences in pancreatic and gut-hormone release between breast-fed and bottle-fed infants have not been documented although these hormones may play a key role in postnatal adaptation. In a study of 77 six-day-old healthy term infants, bottle-fed neonates ('Cow and Gate Premium') had significant changes in plasma-concentrations of insulin, motilin, enteroglucagon, neurotensin, and pancreatic polypeptide after feeding, whereas in breast-fed infants these changes were reduced or absent. Basal levels of gastric inhibitory polypeptide, motilin, neurotensin, and vasoactive intestinal peptide were also higher in the bottle-fed infants than in those who were breast-fed. These findings may partly explain differences in the deposition of subcutaneous fat and in stool frequency between breast-fed and bottle-fed neonates.

Bottle Feeding↗

Effects of pancreatic polypeptide on motilin and circulating metabolites in man.

Pancreatic polypeptide was infused intravenously in healthy fasting subjects at 1 pmol kg-1 (n = 7) and 4 pmol kg-1 min-1 (n = 10) producing plasma PP concentrations of 223 +/- 37 pmol/l (mean +/- SEM) and 891 +/- 64 pmol/l respectively. These levels are similar to and four-fold higher than those seen after a normal mixed breakfast in healthy young adults. In a separate study five healthy subjects ingested a small breakfast during infusion of PP on different days at 1 pmol kg-1 min-1 and 2 pmol kg-1 min-1 respectively. PP at 1 pmol kg-1 min-1 caused a marked reduction in fasting plasma motilin concentrations to 20% of the basal level (p less than 0.001). There were, however, no significant changes in plasma concentrations of insulin, glucagon, gastrin, secretin, enteroglucagon, gastric inhibitory peptide or neurotensin. Despite previous reports possibly implicating PP in metabolism, there were no significant effects on blood levels of glucose, alanine lactate, 3-hydroxybutyrate, glycerol or non-esterified fatty acids, either in the fasting state or after the ingestion of food. Although it seems unlikely that PP is a major hormonal regulator of intermediary metabolism in man, its ability to suppress motilin at physiological concentrations suggests the possibility of an indirect influence on digestive motor function.

Adult↗

Plasma secretin in neonates.

Plasma secretin has been measured in 96 normal 6-day-old term infants and in 158 healthy preterm infants whose mean post-partum ages were 2 1/2, 6, 13 or 24-days. At birth, plasma secretin levels in both term and preterm infants were high compared with those seen in healthy fasting adults (p less than 0.001), but subsequently declined towards adult values. In contrast, preterm infants who had not been fed for the first 6 days of life, had presistently high basal plasma secretin values. In term infants at 6 days of age and in preterm infants up to 13 days, there was no secretin response to a feed. However, by 24 days, preterm infants showed a marked postprandial secretin elevation (p less than 0.02). No correlations were found between plasma secretin concentrations and either blood glucose or plasma insulin concentrations following a feed. Significant adjustments in plasma secretin levels occur in the early weeks of life which may be influenced by enteral feeding.

Adult↗

Plasma pancreatic polypeptide in the human neonate.

Plasma pancreatic polypeptide (PP) concentrations have been studied in 197 healthy term and preterm infants. At birth plasma concentrations were lower than those found in the young fasting adult (p less than 0.01), but by the sixth postnatal day in both term and preterm infants basal concentrations had risen to adult levels. In preterm infants, who were studied at two further postnatal ages, 13 and 24 days, basal plasma PP concentrations peaked at 13 days with levels that were over twice those seen in fasting adults (p less than 0.005). However, the marked PP elevations following feeding that have been reported in adults, were not seen in any of the groups of neonates studied. PP physiology thus appears to differ in neonates and adults. These findings may be relevant to adaptation to postnatal life.

Adult↗

Plasma motilin, gastrin, and enteroglucagon and feeding in the human newborn.

Plasma concentrations of motilin, gastrin, and enteroglucagon were measured in cord blood and during the first 24 days of life before feeding in 45 term and 63 preterm, healthy infants. Levels of these hormones rose steeply after birth, reaching concentrations that were much higher than those in fasting adults. These increases in hormone concentration were not present in a group of 10 preterm infants who had received only intravaenous dextrose from birth because of hyaline membrane disease. Our findings suggest that early enteral feeding may trigger the postnatal increase in plasma concentrations of gut hormones and that this could play an important role in the physiologaical adaptations to extrauterine nutrition.

Fetal Blood↗

Response of plasma pancreatic and gastrointestinal hormones and growth hormone to oral and intravenous glucose and insulin hypoglycaemia in Chagas's disease.

Plasma hormonal responses to insulin hypoglycaemia and to oral and intravenous glucose were investigated in chagasic patients with severe bowel disease and compared with controls matched for age, sex, weight, and race. After intravenous insulin, plasma concentrations of pancreatic glucagon and pancreatic polypeptide (PP) were reduced in the patients with Chagas's disease. These subjects also showed a subnormal rise in plasma insulin after oral glucose. Other hormone responses did not differ significantly from those in the normal controls. These results are compatible with partial denervation of the pancreatic alpha, beta, and PP cells in patients with chronic gastrointestinal Chagas's disease.

Adolescent↗

Neurotensin infusion in man: pharmacokinetics and effect on gastrointestinal and pituitary hormones.

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.

Adult↗

The effect of pirenzepine on meal-stimulated gastrointestinal hormones.

The effects of pirenzepine on the plasma concentrations of gut hormones in the fasting and postprandial states were studied in six healthy subjects. On separate days and in random order, 10 mg pirenzepine, in 2 ml of solvent, or 2 ml saline (0.15 mol/l) were given intravenously 30 min before a standard normal breakfast (2220 kJ). Pirenzepine was not found to affect basal or postprandial levels of insulin, glucagon, gastric inhibitory peptide (GIP), neurotensin, vasoactive intestinal peptide (VIP) or somatostatin. The basal concentration of pancreatic polypeptide (PP) was lowered (p less than 0.05) and the postprandial elevation reduced, though not significantly. While the basal concentration of motilin was also suppressed (p less than 0.05), the postprandial elevation remained unchanged following pirenzepine. The release of enteroglucagon was reduced significantly in the basal and postprandial states (p less than 0.05 and p less than 0.025 respectively). The postprandial gastrin response was prolonged slightly, but insignificantly, by pirenzepine. It is concluded that pirenzepine does not exert any major or unexpected actions on the hormonal control of digestion.

Adult↗

Hormonal abnormalities of the pancreas and gut in cystic fibrosis.

We have investigated the effect of cystic fibrosis on alimentary hormones in 10 children by measuring the pancreatic and gut hormone rsponse to a milk drink. Plasma insulin and gastric inhibitory peptide were both significantly reduced (P < 0.05 and P < 0.005, respectively, at 15 min) in the patients with cystic fibrosis, compared with controls, even though the early glucose rise was greater in the former group (P < 0.05 at 15 min). Fasting levels of pancreatic polypeptide were significantly lower in the fibrocystic children (P < 0.01), and the normal response to milk was completely abolished in these patients (P < 0.001). Fasting plasma enteroglucagon concentrations were grossly abolished in the cystic fibrosis patients (P < 0.001) and these remained elevated throughout the test. No significant differences were seen in basal or postmilk responses of plasma glucagon, gastrin, secretin, vasoactive intestinal peptide, or motilin in cystic fibrosis. It would thus appear that the pancreatic polypeptide cell is more susceptible to the effects of the disease process than the beta or alpha cell in cystic fibrosis. Some aspects of the abnormalities in the gastrointestinal endocrine system were similar to those seen in celiac disease and tropical sprue and may, therefore, effect a similar hormonal response in these patients with cystic fibrosis to those with mucosal damage.

Adolescent↗

Suppression of pancreatic endocrine tumour secretion by long-acting somatostatin analogue.

A new long-acting octapeptide analogue of somatostatin, Des AA1,2,4,5,12,13 D Try8 somatostatin, has been tested in 8 patients with pancreatic endocrine tumours. The analogue given subcutaneously suppressed the tumour-derived hormones in patients with insulinomas, glucagonomas, and gastrinomas for up to 24 h. The prolonged action appeared to be the result of slow release from the injection site. No side-effects were observed. Studies of long-term administration of this new peptide are now warranted.

Adult↗

Plasma trypsin in chronic pancreatitis and pancreatic adenocarcinoma.

We have used a simple and precise radioimmunoassay to measure trypsin in human plasma. Fasting plasma trypsin concentrations were extremely low in patients with chronic pancreatitis with steatorrhoea (5 +/- 2 ng/ml) when compared to healthy controls (86 +/- 7 ng/ml, p less than 0.001). In patients with chronic pancreatitis but no steatorrhoea basal plasma trypsin levels were similar to those of the normal controls (99 +/- 25 ng/ml). A small but significant postprandial rise in plasma trypsin concentrations was observed in normal subjects (mean increment 15 +/- 4%, p less than 0.005, paired t test) but was absent in patients with chronic pancreatitis with steatorrhoea. In contrast to exocrine deficient chronic pancreatitis, other malabsorptive conditions associated with steatorrhoea (active coeliac disease and acute tropical sprue) demonstrated mean fasting trypsin concentrations similar to controls. Patients with adenocarcinoma of the pancreas had basal trypsin concentrations similar to healthy subjects as did patients with adenocarcinoma of the stomach, colon, rectum, brochus, and breast. In some cases measurement of plasma trypsin may be of help in the differential diagnosis of steatorrhoea.

Adenocarcinoma↗

Hypotrypsinaemia in diabetes mellitus.

Plasma trypsin concentrations were measured in 403 fasting diabetics and 106 healthy controls. Basal trypsin concentrations in the normal subjects were 88 +/- 6 ng/ml (mean +/- S.E.M.). Mean plasma trypsin concentrations in diabetics treated with diet alone (n = 74) were 45 +/- 2 ng/ml, while in a group of young (less than 35 years, n = 88) insulin-dependent diabetics, they were very low at 29 +/- 2 ng/ml and these levels were inversely related to insulin dosage. The findings may help in the understanding of the pathophysiological changes in the exocrine pancreas in the diabetic state and may also shed some light on the physiological interrelationship between the endocrine and exocrine pancreas.

Adolescent↗