Ileal Absorption of Tyrosine Conjugated Bile Salts

1985 ◽  
Vol 69 (s12) ◽  
pp. 10P-10P
Author(s):  
C.O. Mills ◽  
S. Iqbal ◽  
E. Elias
2000 ◽  
Vol 63 (10) ◽  
pp. 1369-1376 ◽  
Author(s):  
WILLIAM P. CHARTERIS ◽  
PHILLIP M. KELLY ◽  
LORENZO MORELLI ◽  
J. KEVIN COLLINS

Virtually every antibiotic may cause in vivo alterations in the number, level, and composition of the indigenous microbiotae. The degree to which the microbiotae are disturbed depends on many factors. Although bile may augment antibiotic activity, studies on the effect of bile on the antibiotic susceptibility of indigenous and exogenous probiotic microorganisms are lacking. It was against this background that the antibiotic susceptibility of 37 bile salt–tolerant Lactobacillus and 11 Bifidobacterium isolates from human and other sources was determined in the presence of 0.5% wt/wt oxgall (conjugated bile salts). Oxgall did not affect the intrinsic resistance of lactobacilli to metronidazole (5 μg), vancomycin (30 μg), and cotrimoxazole (25 μg), whereas it resulted in a complete loss of resistance to polymyxin B (300 μg) and the aminoglycosides gentamicin (10 μg), kanamycin (30 μg), and streptomycin (10 μg) for most strains studied (P < 0.001). Oxgall did not affect the intrinsic resistance of bifidobacteria to metronidazole and vancomycin, whereas polymyxin B and co-trimoxazole resistance was diminished (P < 0.05) and aminoglycoside resistance was lost (P < 0.001). Seven lactobacilli, but no bifidobacteria strain, showed unaltered intrinsic antibiotic resistance profiles in the presence of oxgall. Oxgall affected the extrinsic susceptibility of lactobacilli and bifidobacteria to penicillin G (10 μg), ampicillin (10 μg), tetracycline (30 μg), chloramphenicol (30 μg), erythromycin (15 μg), and rifampicin (5 μg) in a source- and strain-dependent manner. Human strain–drug combinations of lactobacilli (P < 0.05) and bifidobacteria (P < 0.01) were more likely to show no change or decreased susceptibility compared with other strain-drug combinations. The antimicrobial activity spectra of polymyxin B and the aminoglycosides should not be considered limited to gram-negative bacteria but extended to include gram-positive genera of the indigenous and transiting microbiotae in the presence of conjugated bile salts. Those lactobacilli (7 of 37) that show unaltered intrinsic and diminished extrinsic antibiotic susceptibility in the presence of oxgall may possess greater upper gastrointestinal tract transit tolerance in the presence of antibiotics.


1986 ◽  
Vol 251 (5) ◽  
pp. G688-G694
Author(s):  
J. L. Goldstein ◽  
L. N. Schmidt ◽  
F. J. Al-Bazzaz ◽  
T. J. Layden

Bile salts have been implicated as a cause of esophageal injury. We examined in vitro the changes in ionic transport of the rabbit esophagus resulting from taurine-conjugated bile salts at neutral pH to define and characterize their actions independent of hydrogen ion. In an Ussing chamber changes in potential difference (PD, mV), short-circuit current (SCC, microA X cm-2) and resistance (R, omega X cm2) resulting from taurocholate (TC), taurodeoxycholate (TDC) and taurochenodeoxycholate (TCDC) were studied. Transport properties were unaffected by TC at 5 and 10 mM. With TDC (5 mM) there was an initial rise in SCC and PD. After 60 min PD and R declined in association with an increase in paracellular permeability as measured by [14C]sucrose flux. TCDC (5.0 and 7.5 mM) caused a sustained rise in PD and SCC with a greater rise seen at 7.5 mM. The rise in SCC after TCDC was secondary to an increase in net sodium absorption as basal net sodium absorption increased threefold from 0.15 +/- 0.03 to 0.44 +/- 0.10 mu eq X cm-2 X h-1. Increased net sodium absorption accounted for 73% of the TCDC-induced rise in SCC. Amiloride (10(-4) M) added to the mucosal solution significantly inhibited this bile salt-induced rise in SCC. We conclude that bile salts alter ionic transport in the esophageal mucosa independent of hydrogen ion. These changes are characterized by an early selective increase in apical membrane cation conductance and with longer exposure, particularly in the presence of more hydrophobic bile salts, there is a marked increase in paracellular conductance.


2005 ◽  
Vol 46 (11) ◽  
pp. 2325-2338 ◽  
Author(s):  
G. Pütz ◽  
W. Schmider ◽  
R. Nitschke ◽  
G. Kurz ◽  
H. E. Blum

1972 ◽  
Vol 139 (1) ◽  
pp. 70-73 ◽  
Author(s):  
D. A. Cook ◽  
L. M. Hagerman ◽  
D. L. Schneider

2013 ◽  
Vol 781-784 ◽  
pp. 1336-1340
Author(s):  
Hui Liu ◽  
Yuan Hong Xie ◽  
Tao Han ◽  
Hong Xing Zhang

Cholesterol-lowering strains were obtained by high throughput screening technology and ortho-phthalaldehyde method. We used oxford cup method to screen again to obtain strains of high yield bile salt hydrolase and illuminate action mechanism ofLactobacillusreducing cholesterol. Screened six strains had the ability of high yield bile salt hydrolase and good ferment ability. The results of identifying bacteria species: strain KTxKL1J1 wereLactobacillus casei, strain Tx wasStreptococcus thermophilus, strain KS4P1 wereLactococcus lactis subsp.lactis, where the last two bacteria were strain of high yield bile salt hydrolase to be few known in literature. This work showed that dissociation bile salts and cholesterol conjuncted sediments by bile salt hydrolase decomposing conjugated bile salts.


1983 ◽  
Vol 65 (1) ◽  
pp. 77-84 ◽  
Author(s):  
A. Chitranukroh ◽  
B. H. Billing

1. A micro-partition centrifugal ultrafiltration technique has been used to monitor the percentage of[14C]glycocholate,[3H]glycochenodeoxycholate and[3H]glycochenodepxycholate-3-sulphate bound to serum proteins of patients with cholestatic liver disease. 2. in comparison with normal individuals the percentage of binding of [14C]glycocholate and, to a lesser extent, of [3H]glycochenodeoxycholate and [3H]glycochenodeoxycholate-3-sulphate was reduced. 3. The binding of [14C]glycocholate was inversely related to the serum bile salt and bilirubin concentrations. in contrast, the binding of [3H]glycochenodeoxycholate and [3H]glycochenodeoxycholate-3-sulphate were not altered by the severity of the cholestasis. 4. Studies in vitro indicated that the reduction in the binding of [14C]glycocholate in cholestatic liver disease was not due to high concentrations of bile salts, unconjugated bilirubin or fatty acids.


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