Abstract
The effects of somatostatin (growth hormone release inhibiting hormone) on basal gastrin were studied in patients suffering from pernicious anaemia and chronic renal and liver disease, and during sequential arginine/insulin-stimulated gastrin release in normal subjects. When basal gastrin concentrations were normal (10-50 pg/ml) in controls and in patients who were in renal and liver failure, somatostatin had no effect on gastrin levels. Raised basal gastrin levels in pernicious anaemia and in 2 cases of chronic renal disease, were significantly inhibited by somatostatin with a half-life (T-half) of 3 to 4 minutes. Arginine infusion caused an insignificant rise in serum gastrin which was unaffected by somatostatin, whereas insulin hypoglycaemia significantly stimulated gastrin release, which was inhibited by somatostatin.
Citation Formats
Le Roith, D, Vinik, A I, Epstein, S, Baron, P, Olkenitzky, M N, and Pimstone, B L.
Somatostatin and serum gastrin in normal subjects and in patients with pernicious anaemia, chronic liver and renal disease.
South Africa: N. p.,
1975.
Web.
Le Roith, D, Vinik, A I, Epstein, S, Baron, P, Olkenitzky, M N, & Pimstone, B L.
Somatostatin and serum gastrin in normal subjects and in patients with pernicious anaemia, chronic liver and renal disease.
South Africa.
Le Roith, D, Vinik, A I, Epstein, S, Baron, P, Olkenitzky, M N, and Pimstone, B L.
1975.
"Somatostatin and serum gastrin in normal subjects and in patients with pernicious anaemia, chronic liver and renal disease."
South Africa.
@misc{etde_5281552,
title = {Somatostatin and serum gastrin in normal subjects and in patients with pernicious anaemia, chronic liver and renal disease}
author = {Le Roith, D, Vinik, A I, Epstein, S, Baron, P, Olkenitzky, M N, and Pimstone, B L}
abstractNote = {The effects of somatostatin (growth hormone release inhibiting hormone) on basal gastrin were studied in patients suffering from pernicious anaemia and chronic renal and liver disease, and during sequential arginine/insulin-stimulated gastrin release in normal subjects. When basal gastrin concentrations were normal (10-50 pg/ml) in controls and in patients who were in renal and liver failure, somatostatin had no effect on gastrin levels. Raised basal gastrin levels in pernicious anaemia and in 2 cases of chronic renal disease, were significantly inhibited by somatostatin with a half-life (T-half) of 3 to 4 minutes. Arginine infusion caused an insignificant rise in serum gastrin which was unaffected by somatostatin, whereas insulin hypoglycaemia significantly stimulated gastrin release, which was inhibited by somatostatin.}
journal = {S. Afr. Med. J.; (South Africa)}
volume = {49:39}
journal type = {AC}
place = {South Africa}
year = {1975}
month = {Sep}
}
title = {Somatostatin and serum gastrin in normal subjects and in patients with pernicious anaemia, chronic liver and renal disease}
author = {Le Roith, D, Vinik, A I, Epstein, S, Baron, P, Olkenitzky, M N, and Pimstone, B L}
abstractNote = {The effects of somatostatin (growth hormone release inhibiting hormone) on basal gastrin were studied in patients suffering from pernicious anaemia and chronic renal and liver disease, and during sequential arginine/insulin-stimulated gastrin release in normal subjects. When basal gastrin concentrations were normal (10-50 pg/ml) in controls and in patients who were in renal and liver failure, somatostatin had no effect on gastrin levels. Raised basal gastrin levels in pernicious anaemia and in 2 cases of chronic renal disease, were significantly inhibited by somatostatin with a half-life (T-half) of 3 to 4 minutes. Arginine infusion caused an insignificant rise in serum gastrin which was unaffected by somatostatin, whereas insulin hypoglycaemia significantly stimulated gastrin release, which was inhibited by somatostatin.}
journal = {S. Afr. Med. J.; (South Africa)}
volume = {49:39}
journal type = {AC}
place = {South Africa}
year = {1975}
month = {Sep}
}