Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Chemotherapy-Induced Nausea and Vomiting: Cannabinoids

Chemotherapy-Induced Nausea and Vomiting: Cannabinoids

Tetrahydrocannabinol (THC) is a phytocannabinoid that primarily interacts with the CB1 receptor, a type of G protein-coupled receptor (GPCR) predominantly in and around the chemoreceptor trigger zone (CTZ) and emetic center. THC also blocks the serotonin receptor activity in the dorsal vagal complex (DVC) by inhibiting serotonin release. THC exerts its anti-emetic effects through these interactions, which are beneficial for patients undergoing chemotherapy.
Two synthetic agonists of THC,...

Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test

Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test

In clinical practice, the direct measurement of hepatic blood flow to evaluate liver function presents significant challenges due to the intricate and specialized nature of the necessary techniques. Consequently, healthcare professionals often rely on empirical estimates derived from thorough patient examinations and liver function tests to gauge liver health. Among the tools at their disposal, the Child–Pugh and MELD scoring systems stand out for their ability to categorize and assess the...

Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow

Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow

Chronic liver disease significantly impacts drug metabolism due to alterations in hepatic blood flow and enzyme accessibility. This disruption affects the body's pharmacokinetics—the movement and processing of drugs within the system. Key enzymes crucial for metabolizing medications become less accessible, changing how drugs are processed and utilized. Furthermore, liver disease influences the synthesis of plasma proteins, such as albumin and globulins, which play critical roles in drug binding...

Chronic Pancreatitis II: Pathophysiology

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...

Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment

Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment

Hepatic impairment, characterized by decreased liver function, does not uniformly mandate adjustments in drug dosage. Whether dosage modifications are necessary depends on various factors related to the drug's metabolism and elimination pathways. If a drug is primarily excreted via the kidneys and bypasses significant hepatic processing, if it undergoes minimal metabolic transformation in the liver, or if it is volatile and primarily expelled through the lungs, dose adjustments may not be...

Cirrhosis II: Pathophysiology

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Unlocking Selenium Chemical Space via a Programmable Synthesis Platform Bearing Cannabinoid Receptor Recognition Motifs.

Journal of the American Chemical Society·2026

Same author

Aquaporin 9 regulates acetaldehyde uptake, alcohol-induced liver injury, and drinking behavior.

Alcohol, clinical & experimental research·2026

Same author

Monlunabant in adults with obesity and metabolic syndrome: Open-label extension of a phase 2a trial.

Diabetes, obesity & metabolism·2026

Same author

A double-blind, randomized, placebo-controlled, phase 2 trial examined the efficacy and safety of monlunabant in adults with diabetic kidney disease.

Kidney international·2026

Same author

Hepatic Aquaporin 8 Promotes Alcohol Consumption and Ameliorates Alcohol-Induced Liver Injury by Facilitating Acetaldehyde Excretion.

International journal of biological sciences·2026

Same author

Leveraging Peripheral CB1 Antagonism in 1,4,5,6-Tetrahydropyridazine-Based Amidine Substituted Sulfonyl Analogs for Treating Metabolic Disorders.

Journal of medicinal chemistry·2025

Search research articles

Related Experiment Video

Updated: Jun 5, 2026

Lipidomics and Transcriptomics in Neurological Diseases

Lipidomics and Transcriptomics in Neurological Diseases

Published on: March 18, 2022

Endocannabinoids in liver disease.

Joseph Tam¹, Jie Liu, Bani Mukhopadhyay

¹National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892-9413, USA.

Hepatology (Baltimore, Md.)

|January 22, 2011

Summary

This summary is machine-generated.

The endocannabinoid system (ECS) plays a role in liver disease. Blocking CB(1) receptors in the liver may treat conditions like cirrhosis and fatty liver, potentially avoiding brain side effects.

More Related Videos

In vivo Liver Endocytosis Followed by Purification of Liver Cells by Liver Perfusion

In vivo Liver Endocytosis Followed by Purification of Liver Cells by Liver Perfusion

Published on: November 10, 2011

Novel In Vivo Micro-Computed Tomography Imaging Techniques for Assessing the Progression of Non-Alcoholic Fatty Liver Disease

Novel In Vivo Micro-Computed Tomography Imaging Techniques for Assessing the Progression of Non-Alcoholic Fatty Liver Disease

Published on: March 24, 2023

Related Experiment Videos

Last Updated: Jun 5, 2026

Lipidomics and Transcriptomics in Neurological Diseases

Lipidomics and Transcriptomics in Neurological Diseases

Published on: March 18, 2022

In vivo Liver Endocytosis Followed by Purification of Liver Cells by Liver Perfusion

In vivo Liver Endocytosis Followed by Purification of Liver Cells by Liver Perfusion

Published on: November 10, 2011

Novel In Vivo Micro-Computed Tomography Imaging Techniques for Assessing the Progression of Non-Alcoholic Fatty Liver Disease

Novel In Vivo Micro-Computed Tomography Imaging Techniques for Assessing the Progression of Non-Alcoholic Fatty Liver Disease

Published on: March 24, 2023

Area of Science:

Hepatology
Endocrinology
Pharmacology

Background:

The endocannabinoid system (ECS), comprising cannabinoid (CB) receptors, endocannabinoids, and associated enzymes, is present in the liver.
Hepatic ECS activation is implicated in the pathology of various liver diseases.

Purpose of the Study:

To investigate the role of the hepatic ECS in liver disease.
To evaluate the therapeutic potential of CB(1) receptor blockade in liver pathologies.

Main Methods:

Review of existing literature on ECS involvement in liver disease.
Analysis of studies using CB(1) blockade in animal models and human patients with liver conditions.

Main Results:

CB(1) receptor activation in cirrhosis contributes to vasodilation and cardiomyopathy, reversible by CB(1) blockade.
In liver fibrosis models, CB(1) receptor activation on hepatic stellate cells is fibrogenic, and blockade slows progression.
Fatty liver, insulin resistance, and dyslipidemias involve peripheral CB(1) receptor activation, including in the liver.

Conclusions:

The hepatic ECS is a significant contributor to liver disease pathogenesis.
CB(1) receptor blockade shows therapeutic promise for cirrhosis, fibrosis, and fatty liver.
Peripherally restricted CB(1) antagonists may mitigate neuropsychiatric side effects, enhancing therapeutic applicability.