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PubMed1978

[Metabolism of somatotropin in severe liver diseases. Influence of the therapeutic administration of a liver extract].

Metabolic Clearance Rate (MCR) and half life of 125I Human Growth Hormone (HGH) have been studied in hepatopathic patients. A clear reduction of MCR and a prolongation of HGH half life have been found in all patients examined. After a 30 day therapy with crude liver extract (F.U. VIII ed.) both MCR and HGH half life have shown a tendency towards normalization. These findings are in agreement with the marked improvement of the clinical state of the patients and with the normalization of the laboratory indexes.

Growth Hormone↗
PubMed1979

Comparison of gastric secretory response in man to duodenal and jejunal liver extract perfusion.

The stomachs of six healthy volunteers were intubated with a Levine tube. In addition, a thin polyethylene tube was placed in the proximal jejunum or in the proximal duodenum. After a 1-h period with no perfusion the intestine was perfused for 2 h with 7% liver extract (LE) (pH 5.5; 380 MOsm/kg water) at a rate of 100 ml/h. In control tests 200 ml of 0.9% physiologic saline solution were used as perfusate. Reflux to the stomach was determined by addition of radioactive B12 to the perfusates. Plasma gastrin, gastric acid, and pepsin levels were measured in 15-min periods. During perfusion of the proximal jejunum only pepsin outputs were increased significantly. During duodenal perfusion of LE, gastric acid and pepsin outputs were increased to 31% and 73% of maximal pentagastrin stimulation, respectively. Controls showed no changes in gastric secretion. Plasma gastrin levels were not elevated after jejunal or duodenal perfusion. These results confirm that the intestinal phase of gastric secretory stimulation does exist in humans. Furthermore, it appears that the major portion of this stimulation originates from the duodenum and is not gastrin-dependent.

Adult↗
PubMed1977

Plasma gastrin and gastric secretory response to duodenal perfusion with liver extract in healthy human subjects.

The stomachs of 8 healthy volunteers were intubated with a Levine tube under radiological control. In addition, a thin polyethylene tube was placed in the proximal duodenum. After a 1-hour period with no perfusion, the duodenum was perfused for two hours with 15% liver extract (LE) (pH 4.5--5.5; 1027 mosm/kg water) at a rate of 100 ml/hour either alone or in combination with intravenous infusion of different doses of exogenous pentagastrin. All subjects were also tested with the tubes in place for 3 hours, but with no perfusion or pentagastrin. Reflux to the stomach was monitored by addition of radioactive B12 to the perfusates. Plasma gastrin, gastric acid, and pepsin were measured in 15-minute periods. During perfusion of the proximal duodenum, where reflux of the perfusates was less than 4%, only a slight and inconstant change in plasma gastrin was seen. Gastric acid and pepsin outputs were increased to approx. 18% and 25% of the maximal pentagastrin stimulation respectively. Whereas 15% LE was shown to release gastrin by antral perfusion however, such release was not found by duodenal perfusion, except where reflux to the antrum was seen. The results suggest that intestinal stimulation of gastric secretion exists, but has not been found to be gastrin dependent in the present investigation.

Duodenum↗
PubMed1986

Effects of secretin antibody on gastric acid inhibition and pancreatic bicarbonate stimulation by acidified liver extract meal in dogs.

Duodenal acidification is known to inhibit gastric H+ secretion while stimulating pancreatic HCO-3 secretion, but the mechanisms of these effects have not been fully explained. This study was designed to determine the role of endogenous and exogenous secretin in gastric inhibition and pancreatic stimulation by an acidified liver extract (LE) meal in conscious dogs prepared with chronic gastric and pancreatic fistulas pretreated with normal serum (control) or anti-secretin serum. In control tests, plasma gastrin and gastric H+ secretion showed a marked rise with LE meals at pH ranging from 7.0 to 4.0, but significantly declined at pH 3.0 and 2.0. Plasma secretin and pancreatic secretion started to rise with LE meals at pHs below 4.5, and both reached peaks at pH 2.0. Exogenous secretin infused at graded doses suppressed plasma gastrin and gastric H+ responses to LE meals at doses of 1.0 and 2.0 U/kg-h, but increased, dose-dependently, plasma secretin and pancreatic HCO-3 starting with a dose of 0.03 U/kg-h. Following the administration of anti-secretin serum, the effects of exogenous secretin on plasma gastrin and secretin levels as well as on gastric and pancreatic secretion were almost completely abolished. The increase in plasma secretin and pancreatic HCO-3 responses to LE meals at pH below 4.5 were also abolished by anti-secretin serum, but the suppression of plasma gastrin level and the inhibition of gastric H+ responses to LE meals at lower pH (3.0 and 2.0) remained virtually unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

Glycosylation of ribonuclease A catalysed by rabbit liver extracts.

Crude extracts of rabbit liver catalyse in vitro the transfer of N-acetylglucosamine from UDP-N-acetylglucosamine to bovine pancreatic ribonuclease A. The enzymic activity is contained in rough endoplasmic reticulum. It has an absolute requirement for a bivalent metal ion: Co-2+ greater than Mn-2+ greater than Ni-2+. Mg-2+ is ineffective. There is enzymic activity in the absence of detergent, but increased activity is observed in the presence of Triton X-100. The site of glycosylation of ribonuclease A is asparagine-34, and glycosylation occurs only at this point. These findings agree with the hypothesis that the sequence Asn-X-Thr(Ser) (where X may be one of a number of types of amino acid) is a necessary, but not sufficient, condition for N-acetylglucosaminylation of a protein-bound asparagine residue.

Acetylglucosamine↗