Related Experiment Video
Updated: Jul 12, 2026

06:10
Extrahepatic Bile Duct and Gall Bladder Dissection in Nine-Day-Old Mouse Neonates
Published on: August 23, 2022
The enterohepatic bile acid axis: from perinatal programming to metabolic collapse
Haiyue Lin1, Jingjing Ye2, Qiufang Bai3
1Department of Dermatology, Tianjin Academy of Traditional Chinese Medicine Affiliated Hospital, Tianjin, China.
Biochemical and Biophysical Research Communications
|July 10, 2026
Summary
The bile acid system
Area of Science:
- Molecular biology
- Developmental biology
- Metabolic research
Background:
- The enterohepatic bile acid system's developmental and adaptive changes are not fully understood.
- Bile acids play critical roles in digestion, metabolism, and signaling pathways.
Purpose of the Study:
- To profile bile acid metabolism genes during liver development, tissue distribution, fasting-refeeding, and in MASH models.
- To define the spatial and temporal regulation of bile acid homeostasis.
Main Methods:
- Gene expression profiling across different physiological states and disease models.
- Analysis of key regulatory loops like FXR-SHP and FGF15 signaling.
Main Results:
- Bile acid synthesis genes activate during perinatal development, with the FXR-SHP loop functional from birth.
- Adult bile acid homeostasis shows hepatic synthesis and ileal reabsorption/FGF15 signaling, indicating spatial compartmentalization.
- Metabolic flexibility during fasting is lost in MASH models, showing FXR-SHP uncoupling or transcriptional collapse.
Conclusions:
- The bile acid metabolic program is precisely regulated across development and space.
- This program is flexibly tuned to nutritional status but is dismantled by chronic metabolic injury.
- Disruption of bile acid homeostasis may be an early event in MASH pathogenesis.
Related Concept Videos
Hepatic Encephalopathy
DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Hepatic Drug Excretion: Enterohepatic Cycling
Enterohepatic cycling involves the active secretion of drugs and their metabolites into the bile via transporters in the canalicular membrane of hepatocytes. This secretion is an integral part of the digestive process, releasing these substances into the gastrointestinal (GI) tract.
Post-release drugs and metabolites can be reabsorbed into the body from the intestine. For conjugated metabolites like glucuronides, reabsorption requires enzymatic hydrolysis by intestinal microflora. This...
Post-release drugs and metabolites can be reabsorbed into the body from the intestine. For conjugated metabolites like glucuronides, reabsorption requires enzymatic hydrolysis by intestinal microflora. This...
Pharmacokinetics in Pediatric Patients: Drug Metabolism
In pediatric care, understanding the nuances of hepatic drug metabolism is crucial, as it significantly differs from that of adults. This divergence is primarily due to the developmental stage of drug-metabolizing enzymes, which affects how medications are processed in the body. In neonates, for instance, the activity of Phase I enzymes—critical for the initial breakdown of drugs—is markedly reduced, functioning at just 20–40% of the levels seen in adults. This reduction poses a challenge in...
Gut-Brain Axis
The gut–brain axis is a bidirectional communication system that connects the gastrointestinal tract and the brain. This interaction is mediated through multiple pathways, including the vagus nerve, hormonal signals, immune responses, and chemical messengers produced by gut microbes.Microbial Contributions to Brain FunctionGut microbiota contributes significantly to brain function by producing neuroactive compounds. These include neuroactive compounds that influence neurotransmitters such as...
Acute Pancreatitis II: Pathophysiology
The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
Chronic Pancreatitis II: Pathophysiology
Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...
