PubMed Health⌕ Search

Biomedical subjects

D Billington

Publications and source records attributed to D Billington.

At least 55 records · Page 3Linked to original sources
PubMed1986

Phospholipid degradation in, and protein content of, rat fistula bile. Contamination of bile with pancreatic juice.

The extent to which pancreatic juice can contaminate bile collected from a rat with a biliary fistula has been investigated by cannulating the bile duct proximal to either the duodenum or the liver, and by stimulating pancreatic flow with secretin. Bile collected via a fistula proximal to the duodenum showed marked pancreatic contamination. Thus, bile collected via a fistula proximal to the duodenum has a higher flow rate, a greater total protein and amylase content and a different polypeptide profile than bile collected via a fistula proximal to the liver. The phospholipid content also differed in that phosphatidylcholine was converted enzymically to lysophosphatidylcholine. Secretin increased bile flow and the biliary output of total protein and amylase when the fistula was proximal to the duodenum, but had no effect upon these parameters when the fistula was proximal to the liver, or in the isolated perfused rat liver.

Amylases↗
PubMed1984

Effect of chenodeoxycholate feeding upon the biliary output of plasma membrane enzymes in the rat.

In model experiments using human erythrocytes, glycochenodeoxycholate caused extensive membrane damage (as judged by release of membrane phospholipid and acetylcholinesterase and by cell lysis) at approximately 10-fold lower concentrations than glycocholate. Chenodeoxycholate feeding had no effect upon the total protein, bile salt or phospholipid concentration of rat bile, although evidence is presented to suggest an expansion of the bile salt pool occurred. Rats fed chenodeoxycholate showed a dose-dependent enrichment of this bile acid in bile; this occurred mainly at the expense of cholate. Chenodeoxycholate feeding resulted in an increased biliary output of the plasma membrane enzymes alkaline phosphatase and 5'-nucleotidase; the hepatic activities of these enzymes were also increased. In contrast, the biliary output and hepatic activities of two other plasma membrane enzymes, alkaline phosphodiesterase I and L-leucine-beta-naphthylamidase, were unaffected by chenodeoxycholate feeding. A greater proportion of all four plasma membrane enzymes studied existed in bile of chenodeoxycholate-fed rats in a "soluble" form (as judged by their remaining in the supernatant on centrifugation of bile). These results are discussed in relation to the origin of plasma membrane enzymes in bile and to the potential toxicity of chenodeoxycholate and its conjugates to the membranes of the hepatobiliary system.

5'-Nucleotidase↗
PubMed1984

Prostacyclin production by confluent and non-confluent human endothelial cells in culture.

Prostacyclin (PGI2) production by cultured human umbilical vein endothelial cells was examined by platelet bioassay and by radioimmunoassay of its stable metabolite 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha). Confluent cultures produced PGI2 in a burst of activity approx. 20 min after changing the growth medium. This occurred in either normal, serum-supplemented growth medium or in balanced salt solution. The mechanical action of changing the growth medium did not appear to be responsible for this burst of PGI2 production. PGI2 production by non-confluent cultures decreased as cell density increased towards confluence. Supplementing the growth medium with arachidonic acid did afford some protection against decreased PGI2 production, whilst the use of conditioned media potentiated this effect. Reduction of cell density by passaging confluent cultures further demonstrated the inverse relationship between PGI2 production and cell density. These results are discussed in relation to the control of PGI2 production in cultured endothelial cells.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Serum alkaline phosphodiesterase I in experimental biliary obstruction in the rat.

Alkaline phosphodiesterase I was present in rat liver at approx. 100-fold greater activity than alkaline phosphatase, and in rat bile at approx. 25-fold greater activity. Rat serum alkaline phosphodiesterase I was increased 6-fold whilst serum alkaline phosphatase was increased only 2-fold 96 h after bile duct ligation. In contrast to alkaline phosphatase, hepatic alkaline phosphodiesterase I was not affected by bile duct ligation, suggesting its raised serum activity was due to bile regurgitation rather than overspill of the enzyme from liver into blood. Gel filtration showed that 8 and 96 h after bile duct ligation the serum contained a high molecular weight form of alkaline phosphodiesterase I. It is suggested that alkaline phosphodiesterase I offers a potentially useful indicator of biliary obstruction in the rat.

Alkaline Phosphatase↗
PubMed1980

Membrane lipid composition and susceptibility to bile salt damage.

Erythrocyte membranes with low sphingomyelin : choline-containing phospholipid ratios haemolyse at low concentrations of the bile salt, glycocholate. Erythrocytes with higher sphingomyelin : choline-containing phospholipid ratios require progressively greater concentrations of the bile salt for lysis. Sublytic concentrations of glycocholate remove phospholipid and acetylcholinesterase from the membranes. Membranes with low sphingomyelin : choline-containing phospholipid ratios lose both particulate (microvesicles of distinct composition) and 'solubilized' material, the particulate form predominating. The proportion of particulate material falls with increase of the membrane sphingomyelin : choline-containing phospholipid ratio and those membranes of highest sphingomyelin : choline-containing phospholipid ratio lose material predominantly in 'solubilized' form. Sheep erythrocytes treated to increase their content of phosphatidylcholine (and thereby reduce their membrane sphingomyelin : choline-containing phospholipid ratio) become more susceptible to lysis by glycocholate. These observations indicate a correlation between membrane lipid composition and the perturbation of membranes with bile salt; they also point to possible features of membranes capable of surviving exposure to the high bile salt concentrations of the biliary tract.

Animals↗
PubMed1980

Effects of bile salts on the plasma membranes of isolated rat hepatocytes.

The conjugated trihydroxy bile salts glycocholate and taurocholate removed approx. 20--30% of the plasma-membrane enzymes 5'-nucleotidase, alkaline phosphatase and alkaline phosphodiesterase I from isolated hepatocytes before the onset of lysis, as judged by release of the cytosolic enzyme lactate dehydrogenase. The conjugated dihydroxy bile salt glycodeoxycholate similarly removed 10--20% of the 5'-nucleotidase and alkaline phosphatase activities, but not alkaline phosphodiesterase activity; this bile salt caused lysis of hepatocytes at approx. 10-fold lower concentrations (1.5--2.0mM) than either glycocholate or taurocholate (12--16mM). At low concentrations (7 mM), glycocholate released these enzymes in a predominantly particulate form, whereas at higher concentrations (15 mM) glycocholate further released these components in a predominantly 'soluble' form. Inclusion of 1% (w/v) bovine serum albumin in the incubations had a small protective effect on the release of enzymes from hepatocytes by glycodeoxycholate, but not by glycocholate. These observations are discussed in relation to the possible role of bile salts in the origin of some biliary proteins.

Animals↗
PubMed1979

Membranes and bile formation. Composition of several mammalian biles and their membrane-damaging properties.

The total content and profile of bile salts and phospholipids are reported for several mammalian biles. Rabbit and guinea-pig biles are characterized by high proportions of conjugated dihydroxy bile salts with respect to trihydroxy bile salts, but contain relatively little phospholipid. Both rabbit and guinea-pig biles exhibit little evidence of hepatic cell damage, even though they are able to cause membrane damage (as evidenced by lysis of human erythrocytes) at low (2--3 mM) concentrations of bile salts; this lytic behaviour is also a property of their predominant bile salts. Addition of phosphatidylcholine to the bile or bile salt is able to decrease the lytic behaviour. Perhaps the most significant observation is that these biles, and their predominant bile salts, are dramatically less lytic towards sheep erythrocytes, indicating that some factor(s) in membrane composition and structure may partly explain the resistance of membranes of the biliary tract to the presence of high concentrations of potentially membrane-damaging bile salts.

Animals↗
PubMed1978

Effects of bile salts of human erythrocytes. Plasma membrane vesiculation, phospholipid solubilization and their possible relationships to bile secretion.

Glycocholate removed approximately 25% of the membrane acetylcholinesterase and 10% of the membrane phospholipid from intact human erythrocytes prior to the onset of cell lysis. At low concentrations (up to 6 mM), glycocholate caused human erythrocytes to become echinocytic and to pinch off microvesicles, whereas at higher concentrations glycocholate also specifically released components from the outer leaflet of the plasma membrane in a 'soluble' form (as defined by their presence in a 150 00 X g/60 min supernatant) and caused the cells to become stomatocytic. Whilst the phospholipdi profile of the 'soluble' material differed from that of the whole membrane, the profile of the microvesicle fraction was similar. The microvesicles were depleted in several membrane proteins with respect to phospholipids. These observations are discussed in relation to the possible role of bile salts in the origins of biliary phospholipid and protein.

Acetylcholinesterase↗
PubMed1978

The effects of hypoglycin on glucose metabolism in the rat. A kinetic study in vivo and [U-14C,2-3H]glucose.

1. The kinetics of glucose metabolism were evaluated in rats deprived of food 15-21 h after the administration of hypoglycaemic doses of hypoglycin (100 mg/kg body wt.) by following changes in the specific radioactivities of 14C and 3H in blood glucose after an intravenous dose of [U-14C,2-3H]glucose [Katz, Rostami & Dunn (1974) Biochem. J. 142, 161-170]. 2. During this time, recycling of glucose through the Cori cycle was virtually abolished, the rate of irreversible disposal of glucose and its total body mass were both decreased by about 70%, whereas there was little effect on the mean transit time for glucose. 3. It was concluded that hypoglycaemia is due to inhibition of gluconeogenesis.

Animals↗
PubMed1977

Topographical dissection of sheep erythrocyte membrane phospholipids by taurocholate and glycocholate.

1. Glycocholate and taurocholate removed significant amounts of membrane phospholipid from intact sheep erythrocytes before lysis of the cells occurred. The pre-lytic extract was enriched in sphingomyelin and correspondingly depleted in phosphatidylserine, phosphatidylinositol and phosphatidylethanolamine when compared to the original membrane. 2. In contrast, the phospholipid profiles of glycocholate and taurocholate extracts of unsealed ghosts, made at the same bile salt concentrations, were similar to that of the whole membrane. 3. These observations are related to the topography of the phospholipids in the membrane and to some aspects of bile formation.

Animals↗