Results 21 to 30 of about 3,456,901 (302)

The role of 11β-hydroxysteroid dehydrogenase type 1 in bile acid homeostasis [PDF]

open access: yes, 2013
Bile acids (BAs) are important modulators of metabolic functions such as lipid, triglyceride and glucose homeostasis. Intrahepatic accumulation of BAs is known to cause liver injury in cholestatic conditions, where normal trans-hepatic BA flow is ...
Penno, Carlos Alberto
core   +1 more source

Bile acid and cholesterol metabolism in atherosclerotic cardiovascular disease and therapy

open access: yesCardiology Plus, 2020
Dysregulation of lipid metabolism is a major factor contributing to atherosclerotic cardiovascular disease (ACVD), which is the number one cause of death in western countries.
John Y. L. Chiang   +3 more
doaj   +1 more source

Regulation of hepatic heme synthesis by drugs, bile acids and nutrition : a transcriptional network regulating [delta]-aminolevulinic acid synthase 1 (ALAS1) [PDF]

open access: yes, 2008
ALAS1 is the rate limiting enzyme of heme synthesis. It is highly inducible in liver in cases of increased heme demand, such as drug metabolism or in inducible hepatic porphyrias.
Peyer, Anne-Kathrin
core   +1 more source

THE METABOLISM OF BILE ACIDS

open access: yesJournal of Biological Chemistry, 1919
"Reprinted from the Journal of biological chemistry, vol. XXXVIII, no. 2, June, 1919." ; "From the George Williams Hooper Foundation for Medical Research, University of California Medical School, San Francisco." ; Thesis t.-p. mounted on cover of [pt.] I. ; Thesis (PH. D.)--University of California, 1919. ; Mode of access: Internet.
M.G. Foster, C.W. Hooper
  +4 more sources

Mutations in SRD5B1 (AKR1D1), the gene encoding Delta(4)-3-oxosteroid 5 beta-reductase, in hepatitis and liver failure in infancy [PDF]

open access: yes, 2003
Background: A substantial group of patients with cholestatic liver disease in infancy excrete, as the major urinary bile acids, the glycine and taurine conjugates of 7alpha-hydroxy-3-oxo-4-cholenoic acid and 7alpha, 12alpha-dihydroxy-3- oxo-4-cholenoic ...
Duran, M.   +17 more
core   +2 more sources

Bile Acid Induced Diarrhoea Pathophysiological and Clinical Aspects [PDF]

open access: yes, 2008
A common cause for referral to gastroenterologists is chronic watery diarrhoea. Approximately 40% of these patients have idiopathic bile acid malabsorption (BAM) – a condition with unknown aetiology.
Bajor, Antal
core   +1 more source

Mutational characterization of the bile acid receptor TGR5 in primary sclerosing cholangitis. [PDF]

open access: yes, 2010
TGR5, the G protein-coupled bile acid receptor 1 (GPBAR1), has been linked to inflammatory pathways as well as bile homeostasis, and could therefore be involved in primary sclerosing cholangitis (PSC) a chronic inflammatory bile duct disease. We aimed to
Bergquist Annika   +186 more
core   +4 more sources

Glycoursodeoxycholic acid regulates bile acids level and alters gut microbiota and glycolipid metabolism to attenuate diabetes

open access: yesGut Microbes, 2023
Accumulating evidence suggests that the bile acid regulates type 2 diabetes mellitus (T2DM) through gut microbiota-host interactions. However, the mechanisms underlying such interactions have been unclear.
Bingting Chen   +7 more
doaj   +1 more source

The Role of Bile in the Regulation of Exocrine Pancreatic Secretion [PDF]

open access: yes, 1992
As early as 1926 Mellanby (1) was able to show that introduction of bile into the duodenum of anesthetized cats produces a copious flow of pancreatic juice.
Riepl, Rudolf L., Lehnert, Peter
core   +1 more source

Crosstalk between FXR and TGR5 controls glucagon-like peptide 1 secretion to maintain glycemic homeostasis

open access: yesLaboratory Animal Research, 2018
Though bile acids have been well known as digestive juice, recent studies have demonstrated that bile acids bind to their endogenous receptors, including Farnesoid X receptor (FXR) and G protein-coupled bile acid receptor 1 (GPBAR1; TGR5) and serve as ...
Hyeonhui Kim, Sungsoon Fang
doaj   +1 more source

Home - About - Disclaimer - Privacy