Results 11 to 20 of about 4,715,473 (300)
Bile acid-axis dysregulation in MASLD/MASH progression: from metabolic mismatch to inflammatory-fibrotic remodeling [PDF]
Frontiers in MedicineMetabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) arise from overlapping metabolic stress, gut-derived inflammatory input, immune activation, and fibrotic remodeling.
Yang Du +7 more
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Preference of Conjugated Bile Acids over Unconjugated Bile Acids as Substrates for OATP1B1 and OATP1B3. [PDF]
PLoS ONE, 2017 Bile acids, the metabolites of cholesterol, are signaling molecules that play critical role in many physiological functions. They undergo enterohepatic circulation through various transporters expressed in intestine and liver.
Takahiro Suga +5 more
doaj +1 more source
Journal of Lipid Research, 2009 In liver and intestine, transporters play a critical role in maintaining the enterohepatic circulation and bile acid homeostasis. Over the past two decades, there has been significant progress toward identifying the individual membrane transporters and unraveling their complex regulation.
Paul A. Dawson, Tian Lan, Anuradha Rao
openaire +3 more sources
The ileal lipid binding protein is required for efficient absorption and transport of bile acids in the distal portion of the murine small intestine. [PDF]
PLoS ONE, 2012 The ileal lipid binding protein (ilbp) is a cytoplasmic protein that binds bile acids with high affinity. However evidence demonstrating the role of this protein in bile acid transport and homeostasis is missing.
Dana Praslickova +6 more
doaj +1 more source
PPARα: A potential therapeutic target of cholestasis
Frontiers in Pharmacology, 2022 The accumulation of bile acids in the liver leads to the development of cholestasis and hepatocyte injury. Nuclear receptors control the synthesis and transport of bile acids in the liver.
Xiaoyin Ye, Tong Zhang, Han Han
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Synthesis, in vitro and in vivo evaluation of 3β-[18F]fluorocholic acid for the detection of drug-induced cholestasis in mice. [PDF]
PLoS ONE, 2017 INTRODUCTION:Drug-induced cholestasis is a liver disorder that might be caused by interference of drugs with the hepatobiliary bile acid transporters. It is important to identify this interference early on in drug development.
Stef De Lombaerde +7 more
doaj +1 more source
The Effects of Bile Acid Feeding on the Development of Ileal Bile Acid Transport [PDF]
Pediatric Research, 1993 Sodium-dependent bile acid uptake is developmentally regulated in the rat ileum. Transport activity is abruptly expressed on postnatal d 17, although the mechanisms controlling this expression are poorly understood. Changes in bile salt metabolism and hepatic transport result in a marked increase in bile flow before postnatal d 17, and thus this study ...
B L, Shneider +3 more
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Bile acid transporters in health and disease [PDF]
Xenobiotica, 2008 In recent years the discovery of a number of major transporter proteins expressed in the liver and intestine specifically involved in bile acid transport has led to improved understanding of bile acid homeostasis and the enterohepatic circulation. Sodium (Na(+))-dependent bile acid uptake from portal blood into the liver is mediated primarily by the Na(
A, Kosters, S J, Karpen
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Bile acid interactions with neurotransmitter transporters
Frontiers in Cellular Neuroscience, 2023 Synthesized in the liver from cholesterol, the bile acids (BAs) primary role is emulsifying fats to facilitate their absorption. BAs can cross the blood-brain barrier (BBB) and be synthesized in the brain. Recent evidence suggests a role for BAs in the gut-brain signaling by modulating the activity of various neuronal receptors and transporters ...
Tiziana Romanazzi +9 more
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Inflammation‐induced cholestasis in cancer cachexia
Journal of Cachexia, Sarcopenia and Muscle, 2021 Background Cancer cachexia is a debilitating metabolic syndrome contributing to cancer death. Organs other than the muscle may contribute to the pathogenesis of cancer cachexia.
Morgane M. Thibaut +20 more
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