The Experts below are selected from a list of 186 Experts worldwide ranked by ideXlab platform
Luis Reuss - One of the best experts on this subject based on the ideXlab platform.
-
Comprehensive Physiology - Salt and Water Transport by Gallbladder Epithelium
Comprehensive Physiology, 2020Co-Authors: Luis ReussAbstract:The sections in this article are: 1 Morphology 2 Basic Transport Functions 3 Mechanisms of Transepithelial Salt Transport 3.1 Basic Electrophysiology of Gallbladder Epithelium 3.2 Paracellular Pathway 3.3 Apical Cell Membrane 3.4 Basolateral Cell Membrane 3.5 Intracellular Ionic Activities 3.6 Transepithelial Ion Fluxes 3.7 Mechanisms of Salt Transport at Apical Membrane 3.8 Mechanisms of Salt Transport at Basolateral Membrane 4 Mechanisms of Transepithelial Water Transport 4.1 Pinocytotic Theory 4.2 Electroosmotic Theory 4.3 Osmotic Theory 5 Conclusions
-
salt and water transport by Gallbladder Epithelium
Comprehensive Physiology, 2011Co-Authors: Luis ReussAbstract:The sections in this article are: 1 Morphology 2 Basic Transport Functions 3 Mechanisms of Transepithelial Salt Transport 3.1 Basic Electrophysiology of Gallbladder Epithelium 3.2 Paracellular Pathway 3.3 Apical Cell Membrane 3.4 Basolateral Cell Membrane 3.5 Intracellular Ionic Activities 3.6 Transepithelial Ion Fluxes 3.7 Mechanisms of Salt Transport at Apical Membrane 3.8 Mechanisms of Salt Transport at Basolateral Membrane 4 Mechanisms of Transepithelial Water Transport 4.1 Pinocytotic Theory 4.2 Electroosmotic Theory 4.3 Osmotic Theory 5 Conclusions
-
muscarinic stimulation of Gallbladder Epithelium i electrophysiology and signaling mechanisms
American Journal of Physiology-cell Physiology, 1993Co-Authors: Guillermo A Altenberg, Muthangi Subramanyam, John S Bergmann, Kenneth M Johnson, Luis ReussAbstract:To understand the effects of acetylcholine (ACh) on fluid-absorbing epithelia, we carried out experiments on Necturus Gallbladder Epithelium. Binding studies with 1-quinuclidinyl[phenyl-4(N)-3H]ben...
-
electrophysiological effects of basolateral na in necturus Gallbladder Epithelium
The Journal of General Physiology, 1992Co-Authors: Guillermo A Altenberg, J S Stoddard, Luis ReussAbstract:In Necturus Gallbladder Epithelium, lowering serosal [Na+] ([Na+]s) reversibly hyperpolarized the basolateral cell membrane voltage (Vcs) and reduced the fractional resistance of the apical membrane (fRa). Previous results have suggested that there is no sizable basolateral Na+ conductance and that there are apical Ca(2+)-activated K+ channels. Here, we studied the mechanisms of the electrophysiological effects of lowering [Na+]s, in particular the possibility that an elevation in intracellular free [Ca2+] hyperpolarizes Vcs by increasing gK+. When [Na+]s was reduced from 100.5 to 10.5 mM (tetramethylammonium substitution), Vcs hyperpolarized from -68 +/- 2 to a peak value of -82 +/- 2 mV (P less than 0.001), and fRa decreased from 0.84 +/- 0.02 to 0.62 +/- 0.02 (P less than 0.001). Addition of 5 mM tetraethylammonium (TEA+) to the mucosal solution reduced both the hyperpolarization of Vcs and the change in fRa, whereas serosal addition of TEA+ had no effect. Ouabain (10(-4) M, serosal side) produced a small depolarization of Vcs and reduced the hyperpolarization upon lowering [Na+]s, without affecting the decrease in fRa. The effects of mucosal TEA+ and serosal ouabain were additive. Neither amiloride (10(-5) or 10(-3) M) nor tetrodotoxin (10(-6) M) had any effects on Vcs or fRa or on their responses to lowering [Na+]s, suggesting that basolateral Na+ channels do not contribute to the control membrane voltage or to the hyperpolarization upon lowering [Na+]s. The basolateral membrane depolarization upon elevating [K+]s was increased transiently during the hyperpolarization of Vcs upon lowering [Na+]s. Since cable analysis experiments show that basolateral membrane resistance increased, a decrease in basolateral Cl- conductance (gCl-) is the main cause of the increased K+ selectivity. Lowering [Na+]s increases intracellular free [Ca2+], which may be responsible for the increase in the apical membrane TEA(+)-sensitive gK+. We conclude that the decrease in fRa by lowering [Na+]s is mainly caused by an increase in intracellular free [Ca2+], which activates TEA(+)-sensitive maxi K+ channels at the apical membrane and decreases apical membrane resistance. The hyperpolarization of Vcs is due to increase in: (a) apical membrane gK+, (b) the contribution of the Na+ pump to Vcs, (c) basolateral membrane K+ selectivity (decreased gCl-), and (d) intraepithelial current flow brought about by a paracellular diffusion potential.
-
Electrophysiological effects of basolateral [Na+] in Necturus Gallbladder Epithelium.
The Journal of General Physiology, 1992Co-Authors: Guillermo A Altenberg, J S Stoddard, Luis ReussAbstract:In Necturus Gallbladder Epithelium, lowering serosal [Na+] ([Na+]s) reversibly hyperpolarized the basolateral cell membrane voltage (Vcs) and reduced the fractional resistance of the apical membrane (fRa). Previous results have suggested that there is no sizable basolateral Na+ conductance and that there are apical Ca(2+)-activated K+ channels. Here, we studied the mechanisms of the electrophysiological effects of lowering [Na+]s, in particular the possibility that an elevation in intracellular free [Ca2+] hyperpolarizes Vcs by increasing gK+. When [Na+]s was reduced from 100.5 to 10.5 mM (tetramethylammonium substitution), Vcs hyperpolarized from -68 +/- 2 to a peak value of -82 +/- 2 mV (P less than 0.001), and fRa decreased from 0.84 +/- 0.02 to 0.62 +/- 0.02 (P less than 0.001). Addition of 5 mM tetraethylammonium (TEA+) to the mucosal solution reduced both the hyperpolarization of Vcs and the change in fRa, whereas serosal addition of TEA+ had no effect. Ouabain (10(-4) M, serosal side) produced a small depolarization of Vcs and reduced the hyperpolarization upon lowering [Na+]s, without affecting the decrease in fRa. The effects of mucosal TEA+ and serosal ouabain were additive. Neither amiloride (10(-5) or 10(-3) M) nor tetrodotoxin (10(-6) M) had any effects on Vcs or fRa or on their responses to lowering [Na+]s, suggesting that basolateral Na+ channels do not contribute to the control membrane voltage or to the hyperpolarization upon lowering [Na+]s. The basolateral membrane depolarization upon elevating [K+]s was increased transiently during the hyperpolarization of Vcs upon lowering [Na+]s. Since cable analysis experiments show that basolateral membrane resistance increased, a decrease in basolateral Cl- conductance (gCl-) is the main cause of the increased K+ selectivity. Lowering [Na+]s increases intracellular free [Ca2+], which may be responsible for the increase in the apical membrane TEA(+)-sensitive gK+. We conclude that the decrease in fRa by lowering [Na+]s is mainly caused by an increase in intracellular free [Ca2+], which activates TEA(+)-sensitive maxi K+ channels at the apical membrane and decreases apical membrane resistance. The hyperpolarization of Vcs is due to increase in: (a) apical membrane gK+, (b) the contribution of the Na+ pump to Vcs, (c) basolateral membrane K+ selectivity (decreased gCl-), and (d) intraepithelial current flow brought about by a paracellular diffusion potential.
G Kottra - One of the best experts on this subject based on the ideXlab platform.
-
the forskolin induced opening of tight junctions in xenopus Gallbladder Epithelium is mediated by protein kinase c
Cellular and Molecular Biology, 2003Co-Authors: G Kottra, C VankAbstract:The effects of protein kinase A (PKA)-mediated and protein kinase C (PKC)-mediated stimulation on the tight junctions of the moderately tight Xenopus Gallbladder Epithelium have been investigated. Transepithelial impedance and DC voltage divider ratio measurements in Ussing-type chambers were used to calculate the cell membrane and tight junction resistances in the stimulated state. Under control conditions the TE resistance was used as a lowest estimate of tight junction resistance. Stimulation of PKA by forskolin and theophyllin as well as stimulation of PKC by phorbol dibutyrate lowered the TE resistance mainly via the reduction of the tight junctional resistance. PKA stimulation opened, in addition, an apical Cl - -selective conductance. The paracellular pathway activated by PKA or PKC did not discriminate between small anions and cations. The effects of PKA stimulation could be blocked by the selective inhibition of PKA (with H89) or of PKC (with bisindolylmaleimide). By contrast, the PKC-evoked effects were insensitive to H89, showing that the effects of PKA on the paracellular pathway were mediated by PKC.
-
protein kinase inhibitor h7 prevents the decrease of tight junction resistance induced by serosal ca2 removal in necturus Gallbladder Epithelium
Cellular Physiology and Biochemistry, 1995Co-Authors: G KottraAbstract:Changes of the tight junction resistance (Rj) of the Necturus Gallbladder Epithelium in response to Ca2+ removal from the bath solutions were investigated by conventional electrophysiological methods and two-dimensional cable analysis. Luminal superfusion with Ca2+-free solution left Rj almost unchanged, while serosal removal of Ca2+ induced a slow decrease of Rj from 155 ± 10 to 25 ± 6 Ωcm2 (n = 10) within 2 h. Simultaneously the apical membrane resistance decreased while the basolateral membrane resistance as well as the gap junction resistance increased. Application of the protein kinase inhibitor H7 (50 µmol/l) blocked these resistance changes. Similar protective effects of H7 on the transepithelial resistance (Rt) were previously observed on MDCK cells [Citi: J Cell Biol 1992; 117:169]. In contrast, 5 µmol/l chelerythrine chloride, a specific blocker of the protein kinase C, did not prevent the decrease of Rj induced by serosal removal of Ca2+. These results indicate that the integrity of the tight junctions of Necturus Gallbladder Epithelium depends on the serosal, but not on the luminal presence of Ca2+ and that the resistance decline includes a process that can be inhibited by H7, but not by chelerythrine chloride.
-
calcium is not involved in the camp mediated stimulation of cl conductance in the apical membrane of necturus Gallbladder Epithelium
Pflügers Archiv: European Journal of Physiology, 1995Co-Authors: G KottraAbstract:The permeability properties of the forskolinstimulated Cl− conductance in the apical membrane of Necturus Gallbladder Epithelium and the possible participation of intracellular Ca2+ in its stimulation have been investigated. The anion selectivity sequence as derived from biionic potential measurements (SCN− > I− ≈ NO 3 − > Br− > Cl− ≫ ISE−) differed from the sequence derived from measurements of apical membrane resistance (NO 3 − ≈ Br− ≈ Cl− > SCN− > I− ≈ ISE−). Accordingly, the conductance was inhibited by SCN− and I− which, from the potential measurements, appeared to be more permeable than Cl−. This finding agrees with observations of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl− channel reported recently. However, none of the commonly used Cl− channel blockers, such as 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid (DIDS), anthracene-9-carboxylic acid (9-AC) and glibenclamide reduced this conductance in Necturus Gallbladder. In contrast to the situation in most other epithelia, elevation of intracellular Ca2+ concentration ([Ca2+]i) by ionomycin stimulated only K+ conductance and not that of Cl− in the apical cell membrane. Chelation of intracellular Ca2+ did not prevent the stimulation of Cl− conductance by forskolin. This indicates that [Ca2+]i does not have even a permissive role in the cyclic adenosine monophosphate-(cAMP)-mediated stimulation process, as would have been expected if exocytosis was involved. Further evidence against the involvement of exocytosis in the stimulation process came from the observation that the stimulation was not associated with an increase in apical membrane capacitance and was not suppressed by disruption of the cytoskeleton by preincubation of the tissue with cytochalasin D. The data indicate that Necturus Gallbladder Epithelium contains homologues of the CFTR Cl− channel which reside permanently in the apical cell membrane and which can be stimulated by a cAMP-dependent phosphorylation process without involvement of cell Ca2+ or exocytosis.
-
Calcium is not involved in the cAMP-mediated stimulation of Cl− conductance in the apical membrane of Necturus Gallbladder Epithelium
Pflügers Archiv: European Journal of Physiology, 1995Co-Authors: G KottraAbstract:The permeability properties of the forskolinstimulated Cl− conductance in the apical membrane of Necturus Gallbladder Epithelium and the possible participation of intracellular Ca2+ in its stimulation have been investigated. The anion selectivity sequence as derived from biionic potential measurements (SCN− > I− ≈ NO 3 − > Br− > Cl− ≫ ISE−) differed from the sequence derived from measurements of apical membrane resistance (NO 3 − ≈ Br− ≈ Cl− > SCN− > I− ≈ ISE−). Accordingly, the conductance was inhibited by SCN− and I− which, from the potential measurements, appeared to be more permeable than Cl−. This finding agrees with observations of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl− channel reported recently. However, none of the commonly used Cl− channel blockers, such as 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid (DIDS), anthracene-9-carboxylic acid (9-AC) and glibenclamide reduced this conductance in Necturus Gallbladder. In contrast to the situation in most other epithelia, elevation of intracellular Ca2+ concentration ([Ca2+]i) by ionomycin stimulated only K+ conductance and not that of Cl− in the apical cell membrane. Chelation of intracellular Ca2+ did not prevent the stimulation of Cl− conductance by forskolin. This indicates that [Ca2+]i does not have even a permissive role in the cyclic adenosine monophosphate-(cAMP)-mediated stimulation process, as would have been expected if exocytosis was involved. Further evidence against the involvement of exocytosis in the stimulation process came from the observation that the stimulation was not associated with an increase in apical membrane capacitance and was not suppressed by disruption of the cytoskeleton by preincubation of the tissue with cytochalasin D. The data indicate that Necturus Gallbladder Epithelium contains homologues of the CFTR Cl− channel which reside permanently in the apical cell membrane and which can be stimulated by a cAMP-dependent phosphorylation process without involvement of cell Ca2+ or exocytosis.
-
barium blocks cell membrane and tight junction conductances in necturus Gallbladder Epithelium experiments with an extended impedance analysis technique
Pflügers Archiv: European Journal of Physiology, 1990Co-Authors: G Kottra, E. FrömterAbstract:The site and concentration dependence of the blocking effect of Ba2+ onNecturus Gallbladder Epithelium has been investigated. A new approach was used which combines time-dependent electrical cell coupling analysis with intermittently performed measurements of transepithelial and apparent intracellular impedance. From the coupling pulse data the sum of apical and basolateral membrane conductances is obtained, which is then held constant during fitting of the impedance data. This combination technique yields more reliable estimates of apical and basolateral membranes resistances (Ra,Rbl) and of tight junction resistance (Rj) than our previous impedance analysis technique. Using the new approach we have found that luminal Ba2+ concentrations between 0.5 and 1.0 mmol/l increaseRa with saturation-type kinetics without affectingRbl andRj, while higher luminal Ba2+ concentrations progressively increaseRj. Corresponding effects were observed under serosal Ba2+. The results validate the new impedance analysis approach and demonstrate that millimolar concentrations of Ba2+ block tight junction conductances. Accordingly, Ba2+ can no longer be considered a tool to exclusively alter cell membrane resistances in epithelia.
J. M. Winterhager - One of the best experts on this subject based on the ideXlab platform.
-
transcellular bicarbonate transport in rabbit Gallbladder Epithelium mechanisms and effects of cyclic amp
Pflügers Archiv: European Journal of Physiology, 1990Co-Authors: K. U. Petersen, Frank Wehner, J. M. WinterhagerAbstract:HCO3 permeation through rabbit Gallbladder Epithelium has been investigated in vitro using voltage-clamp, pH-stat and microelectrode techniques. Mucosa-to-serosa flux of HCO3 (≈4.9 μmol cm−2h−1) was dependent on luminal Na and inhibited by amiloride (1 mmol/l, luminal bath), methazolamide (0.1 mmol/l, both sides), and ouabain (30 μmol/l, serosal bath). Maximal rates of serosa-to-mucosa flux of HCO3 (≈2.8 μmol cm−2h−1) required serosal Na and mucosal Cl. This flux was inhibited by ouabain, 4-acetamido-4′-isothiocyanato-stilbene-2,2′-disulfonic acid (1 mmol/l, serosal bath), and 5-nitro-2-(3-phenylpropylamino)-benzole acid (0.1 mmol/l, luminal bath). Ineffective were methazolamide (0.1 mmol/l, both sides) and amiloride (1 mmol/l, serosal bath). 8-Br-cAMP (1 mmol/l, serosal bath) largely inhibited the absorptive and moderately stimulated the secretory flux. In tissue conductance, short-circuit current, and transmural voltage prostaglandin E1 (1 μmol/l, serosal bath) and 8-Br-cAMP caused moderate to negligible increases. No significant alterations of apical membrane potential (≈ −65 mV) and the apparent ratio of membrane resistances (Ra/Rb;≈1.9) were found. Cell membranes responded to luminal Cl removal mostly with a slow hyperpolarization that was mitigated by 8-Br-cAMP or, in some cases, converted into a small, transient depolarization. Our results are best explained by transcellular HCO3 transport in both directions. In secretion, basolateral HCO3 entry occurs by some form of co-transport with Na, and apical exit by Cl/HCO3 exchange. cAMP opens no major electrodiffusive pathway for apical anion efflux. In absorption, HCO3 import from the lumen into the cell is secondary to cAMP-sensitive Na/H exchange.
-
Naloxone-insensitive transport effects of loperamide in guinea-pig Gallbladder Epithelium
European Journal of Pharmacology, 1990Co-Authors: Frank Wehner, J. M. Winterhager, K. U. PetersenAbstract:The effects of the antidiarrheal drug, loperamide, on HCO3 and Na transport across guinea-pig Gallbladder Epithelium were investigated using Ussing-chamber methods. Under basal conditions, mucosal loperaide (10−4 mol/1) moderately lowered both the absorptive (JmsHCO3) and the secretory HCO3 flux (JsmHCO3) (pH-stat method), most likely by changing paracellular HCO3 flow. Exposure to serosal prostaglandin E1 (10−6 mol/1) aboplished Na absorption and turned HCO3 secretion electrogenic. The associated short-circuit current (Isc) was inhibited by loperamide in a concentration-dependent manner; mucosal addition (threshold at 3 × 10−6 mol/l) of the drug was more effective. Inhibition of Isc was related to a decrease in JsmHCO3, but exceeded the drop in JnetHCO3. The effects on JsmHCO3 and Isc were mimicked by [Met5]enkephalin. Naloxone (10−6 mol/l) was unable to influence the effects of loperamide and [Met5]enkephalin on Isc. There were no pro-absorptive effects of loperamide on unidirectional Na fluxes. We conclude that antisecretory properties of loperamide are solely due to inhibition of electrogenic HCO3 secretion, an effect unrelated to opiate receptor binding.
Joseph T. Walsh - One of the best experts on this subject based on the ideXlab platform.
-
Er:YAG laser ablation of prairie dog Gallbladder Epithelium for the prevention of gallstones
Lasers in Surgery and Medicine, 1994Co-Authors: Steven R. Visuri, Jay B. Prystowsky, Joseph T. WalshAbstract:We hypothesized that laser ablation of Gallbladder Epithelium would prevent gallstone formation in prairie dogs. An Er:YAG laser (λ = 2.94 μm) was used to ablate the Gallbladder Epithelium of 24 prairie dogs; 20 sham-irradiated and 12 non-operated prairie dogs served as controls. Prairie dogs were sacrificed at time periods of 4 days, 2 weeks, and 8–12 weeks and evaluated for the presence of gallstones and cholesterol crystals. Laser-irradiated Gallbladders demonstrated a lower rate of gallstone formation at 8–12 weeks than the sham-irradiated Gallbladders (39% vs. 79%: P
-
er yag laser ablation of prairie dog Gallbladder Epithelium for the prevention of gallstones
Lasers in Surgery and Medicine, 1994Co-Authors: Steven R. Visuri, Jay B. Prystowsky, Joseph T. WalshAbstract:: We hypothesized that laser ablation of Gallbladder Epithelium would prevent gallstone formation in prairie dogs. An Er:YAG laser (lambda = 2.94 microns) was used to ablate the Gallbladder Epithelium of 24 prairie dogs; 20 sham-irradiated and 12 non-operated prairie dogs served as controls. Prairie dogs were sacrificed at time periods of 4 days, 2 weeks, and 8-12 weeks and evaluated for the presence of gallstones and cholesterol crystals. Laser-irradiated Gallbladders demonstrated a lower rate of gallstone formation at 8-12 weeks than the sham-irradiated Gallbladders (39% vs. 79%: P < .02). Crystal formation, however, was not different between laser-irradiated (88%) and sham-irradiated (100%) animals. The laser-irradiated group had less Epithelium than the non-operated group at all time periods (P < or = .002) and compared to the sham-irradiated group at 4 days and 8-12 weeks (P < or = .001). These data suggest that laser ablation of Gallbladder Epithelium can reduce the rate of gallstone formation although this effect may be temporary.
Hyun Joo Jang - One of the best experts on this subject based on the ideXlab platform.
-
pravastatin activates pparα pparγ expression in the liver and Gallbladder Epithelium of hamsters
Hepatobiliary & Pancreatic Diseases International, 2011Co-Authors: Seok Ho Dong, Min Ho Choi, Hyun Joo JangAbstract:Background Our earlier study with cultured Gallbladder epithelial cells demonstrated that statins (HMG-CoA reductase inhibitors) activate the expression of PPARα and PPARγ, consequently blocking the production of pro-inflmmatory cytokines. The present study used hamsters to investigate the effects of pavastatin on PPARα/PPARγ expression in the liver and Gallbladder Epithelium, and to determine whether pravastatin suppresses cholesterol crystal formation in the Gallbladder. Methods A total of 40 Golden Syrian male hamsters (4 weeks old) were randomly assigned to four groups (basal diet control; basal diet+pavastatin; high cholesterol diet; high cholesterol diet+pravastatin). All hamsters were 11 weeks old at the end of the experiment. The liver, Gallbladder and bile were harvested. Immunohistochemical staining and Western blotting for PPARα and PPARγ were performed in the liver and Gallbladder. A drop of fresh bile was examined for cholesterol crystals under a microscope. Results In the Gallbladder and liver of the hamsters, pravastatin activated the PPARα and PPARγ expression of Gallbladder epithelial cells and hepatocytes, and particularly the response of PPARγ was much stronger than that of PPARα. Pravastatin suppressed the formation of cholesterol gallstones or crystals in the Gallbladder. Conclusion Pravastatin is an effective medication to activate PPARs (especially PPARγ) in the liver and the Gallbladder Epithelium of hamsters, and contributes to the prevention of gallstone formation.
-
Pravastatin Activates PPARα/PPARγ Expression in the Liver and Gallbladder Epithelium of Hamsters
Hepatobiliary & Pancreatic Diseases International, 2011Co-Authors: Seok Ho Dong, Min Ho Choi, Hyun Joo JangAbstract:Background Our earlier study with cultured Gallbladder epithelial cells demonstrated that statins (HMG-CoA reductase inhibitors) activate the expression of PPARα and PPARγ, consequently blocking the production of pro-inflmmatory cytokines. The present study used hamsters to investigate the effects of pavastatin on PPARα/PPARγ expression in the liver and Gallbladder Epithelium, and to determine whether pravastatin suppresses cholesterol crystal formation in the Gallbladder. Methods A total of 40 Golden Syrian male hamsters (4 weeks old) were randomly assigned to four groups (basal diet control; basal diet+pavastatin; high cholesterol diet; high cholesterol diet+pravastatin). All hamsters were 11 weeks old at the end of the experiment. The liver, Gallbladder and bile were harvested. Immunohistochemical staining and Western blotting for PPARα and PPARγ were performed in the liver and Gallbladder. A drop of fresh bile was examined for cholesterol crystals under a microscope. Results In the Gallbladder and liver of the hamsters, pravastatin activated the PPARα and PPARγ expression of Gallbladder epithelial cells and hepatocytes, and particularly the response of PPARγ was much stronger than that of PPARα. Pravastatin suppressed the formation of cholesterol gallstones or crystals in the Gallbladder. Conclusion Pravastatin is an effective medication to activate PPARs (especially PPARγ) in the liver and the Gallbladder Epithelium of hamsters, and contributes to the prevention of gallstone formation.
