Biomedical subjects
R G Long
Publications and source records attributed to R G Long.
Effect of neurotensin on gastric function in man.
Neurotensin is a peptide recently discovered in the human ileum and it is released into plasma after ingestion of food. Neurotensin was infused intravenously into 12 healthy volunteers at a mean dose of 2.4 pmol/kg/min, the mean rise in plasma levels being 89 +/- 8 pmol/l. An inhibition of both gastric acid and pepsin output, and also a delay in gastric emptying of oral glucose, were observed. Neurotensin may therefore have a physiological role in modulating gastric function in man.
Neural and hormonal peptides in rectal biopsy specimens from patients with Chagas' disease and chronic autonomic failure.
The neural and hormonal peptide content of rectal biopsy specimens from 10 patients with chronic autonomic failure, 10 patients with chronic gastrointestinal Chagas' disease, and 13 controls was studied with radioimmunoassay and immunocytochemistry. In the patients with Chagas' disease the mean concentrations of rectal vasoactive intestinal polypeptide, enteroglucagon, substance P, and somatostatin were all less than half of those in controls and in patients with chronic autonomic failure. Immunocytochemistry revealed a considerable reduction in the number and immunostaining of the peptide-containing cells and nerves. Concentrations of regulatory peptides in the rectum are thus reduced in association with intrinsic but not extrinsic autonomic neuropathy.
Endocrine aspects of liver disease.
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Effect of conjugated and unconjugated hyperbilirubinaemia on the plasma 25-hydroxy-vitamin D response to ultraviolet radiation in the rat.
1. Vitamin D deficiency was induced in anicteric Wistar rats, Wistar rats before common bile-duct ligation was performed and Gunn rats with unconjugated hyperbilirubinaemia. 2. The effect of ultraviolet radiation on plasma concentrations of 25-hydroxy-vitamin D was studied in a group of control anicteric Wistar rats (n = 11), Wistar rats 8 days after common bile-duct ligation (n = 7) with conjugated hyperbilirubinaemia and in Gunn rats (n = 11). 3. The plasma 25-hydroxy-vitamin D response to ultraviolet radiation was similar in the three groups. 4. It is suggested that neither conjugated nor unconjugated hyperbilirubinaemia prevent cutaneous vitamin D3 synthesis or 25-hydroxylation in the rat.
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.
Hepatic osteodystrophy: outlook good but some problems unsolved.
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The peptidergic system in Chagas's disease [proceedings].
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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.
Intestinal absorption of cholecalciferol in alcoholic liver disease and primary biliary cirrhosis.
The intestinal absorption of (3H)cholecalciferol was studied in five patients with alcoholic liver disease, six patients with primary biliary cirrhosis, and 15 healthy subjects. The rate of appearance in plasma of (3H)cholecalciferol after oral ingestion and the subsequent appearance of (3H) polar metabolites in the alcoholic subjects were similar to those in the healthy subjects. In subjects with primary biliary cirrhosis the rate of appearance in plasma of (3H)cholecalciferol was significantly reduced. The rate of appearance of labelled polar metabolites of cholecalciferol was also lower in this group, suggesting that increased removal of labelled vitamin by conversion into more polar metabolites could not account for the reduced plasma (3H)cholecalciferol response. It is suggested that intestinal absorption of cholecalciferol is usually normal in alcoholic liver disease but impaired in primary biliary cirrhosis. Hepatic 25-hydroxylation is normal in alcoholic liver disease but may be defective in primary biliary cirrhosis.
Vitamin D in chronic liver disease.
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Components necessary for a continuum of services to deaf-blind individuals.
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Phosphate metabolism in chronic liver disease.
Phosphate metabolism was investigated in 26 patients with a spectrum of liver diseases and mean fasting plasma phosphate concentrations were in the low normal range. A standard oral load of phosphate was used to test absorption and was subnormal in the majority of patients with large bile-duct obstruction and alcoholic liver disease. Subnormal results were also seen in patients with primary biliary cirrhosis and cirrhosis secondary to chronic active hepatitis. These abnormalities appeared to be related to vitamin-D deficiency. Tubular reabsorption of phosohate was markedly reduced in 3 of 14 patients. The therapeutic implications of phosphate status in liver disease are important.
Plasma vitamin D-binding globulin in vitamin D deficiency, pregnancy and chronic liver disease.
Plasma concentrations of vitamin D-binding globulin were measured by radial immunodiffusion in healthy subjects, pregnancy, and during oestrogen therapy. Subjects with disorders of vitamin D metabolism (dietary deficiency, malabsorption, anticonvulsant therapy, chronic liver disease) were also studied. Neither sex nor age influenced the plasma vitamin D-binding globulin concentration in healthy subjects, but there was a significant increase in concentration during pregnancy and oestrogen therapy. Elevated levels were found in vitamin D deficient elderly but not younger subjects, while levels in subjects with chronic liver disease were significantly reduced. Normal levels of vitamin D-binding globulin were present in hypervitaminosis D and no vitamin D-binding globulin was detected in human milk. No correlation was observed between plasma 25-hydroxycholecalciferol levels and plasma vitamin D-binding globulin concentrations.
Formation of vitamin D metabolites from 3H- and 14C-radiolabelled vitamin D-3 in chronic liver diseases.
Four of the eight patients studied were vitamin D replete and 4 vitamin D depleted as judged by serum 25-hydroxy vitamin D (25-OHD) concentration. Three of the 4 vitamin D depleted patients (including 2 with histological osteomalacia) formed radioactive 1,25-dihydroxycholecalciferol. One of the four vitamin D replete patients formed 1,25-dihydroxycholecalciferol but all formed 24,25-dihydroxycholecalciferol. This study suggests that patients with liver disease form dihydroxy vitamin D metabolites in an appropriate manner.
Plasma calcium and magnesium fractions in liver disease.
Plasma calcium and magnesium fractions were measured in 51 patients with either hepatocellular or biliary disease. The fractions were found to be only minimally deranged. Plasma albumin correlated with total calcium and with the protein bound and ionized fractions. Abnormalities of plasma calcium or magnesium fractions are unlikely to play a role in the pathogenesis of the osteomalacia seen in chronic biliary disease.
Parenteral 1,25-dihydroxycholecalciferol in hepatic osteomalacia.
Despite regular long-term parenteral vitamin D2 treatment, four patients with biliary cirrhosis had multiple symptoms of bone disease and bone biopsy specimens showed osteomalacia without osteoporosis. Three patients also had a proximal myopathy. Plasma calcium values (after correction for albumin), phosphorus, magnesium, and serum 25-hydroxy-vitamin D were within normal limits. Treatment with 1,25-dihydroxy-cholecalciferol (1,25-(OH)2D3) relieved symptoms in three of the four patients and improved those in the fourth. Histological examination of bone showed improvement in all four patients, but serum and urinary biochemical changes were not pronounced. We conclude that 1,25-(0H)2D3 treatment has a beneficial effect on bone and muscle in hepatic osteomalacia, either because vitamin D 1-hydroxylation fails in biliary cirrhosis or because hepatic osteomalacia is resistant to vitamin D2 metabolites.