Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Overview of Lipid Metabolism01:24

Overview of Lipid Metabolism

7.0K
Lipid metabolism is a crucial process in the human body that involves the synthesis and degradation of lipids. This process is essential for energy production, cell membrane formation, and hormone production, among other functions.
Lipolysis: The Breakdown of Lipids:
Lipolysis is the process of breaking down lipids, particularly triglycerides, into glycerol and fatty acids. This process typically occurs in the adipose tissue and is triggered by various hormones, including glucagon and...
7.0K
Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow01:26

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

386
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...
386
Necrosis01:16

Necrosis

5.3K
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
5.3K
Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test01:22

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

275
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...
275
Effect of Hepatic Disease on Pharmacokinetics: Active Drug, Metabolite and Fraction of Metabolized Drug01:14

Effect of Hepatic Disease on Pharmacokinetics: Active Drug, Metabolite and Fraction of Metabolized Drug

360
In pharmacotherapy, monitoring drug concentrations is paramount, especially for drugs whose therapeutic effects hinge on both the active compound and its metabolite. Hepatic impairment profoundly influences drug potency by altering liver function. If the drug is more potent than its metabolite, impaired liver function amplifies drug activity due to elevated drug concentration levels. Conversely, if the metabolite holds greater potency, diminished liver function diminishes drug activity by...
360
Liver Physiology01:30

Liver Physiology

3.8K
The liver, an essential organ in the human body, performs over 200 vital functions that can be broadly categorized into metabolic, hematological, endocrine regulation, and bile production.
Metabolic Regulation:
The liver is the central organ involved in regulating blood composition. It stabilizes blood glucose levels, maintaining them within the range of  70–110 mg/dL. When these levels drop, the liver breaks down glycogen reserves and releases glucose into the bloodstream. It can...
3.8K

You might also read

Related Articles

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

Sort by
Same author

Stearoyl-CoA desaturase 5 (SCD5) in lipid remodeling: From molecular control to pathophysiology.

Journal of lipid research·2026
Same author

Fine-Tuning of the Endoplasmic Reticulum Stress Response Mechanism Plays a Key Role in Cellular Survival-A Mathematical Study.

International journal of molecular sciences·2025
Same author

Dynamically chiral phosphonic acid-type metallo-β-lactamase inhibitors.

Communications chemistry·2025
Same author

The Importance of Edible Medicinal Mushrooms and Their Potential Use as Therapeutic Agents Against Insulin Resistance.

International journal of molecular sciences·2025
Same author

Development of Novel Imipridones with Alkyne- and Triazole-Linked Warheads on the Tricyclic Skeleton, Showing Superior Ability to Eradicate PANC-1 and Fadu Cells Compared to ONC201.

International journal of molecular sciences·2024
Same author

Fragility of ER homeostatic regulation underlies haploid instability in human somatic cells.

The Journal of biological chemistry·2024

Related Experiment Video

Updated: May 6, 2026

Author Spotlight: Establishing MASLD Cell Models for Investigating Disease Mechanisms and the Lipid-Lowering Effects of Koumiss
07:03

Author Spotlight: Establishing MASLD Cell Models for Investigating Disease Mechanisms and the Lipid-Lowering Effects of Koumiss

Published on: July 19, 2024

1.9K

Lipotoxicity in the liver.

Veronika Zámbó1, Laura Simon-Szabó, Péter Szelényi

  • 1Veronika Zámbó, Laura Simon-Szabó, Péter Szelényi, Éva Kereszturi, Gábor Bánhegyi, Miklós Csala, Department of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, H-1444 Budapest, Hungary.

World Journal of Hepatology
|November 2, 2013
PubMed
Summary

Obesity drives non-alcoholic fatty liver disease (NAFLD). Saturated fatty acids, not triglycerides, cause liver injury by inducing oxidative stress and endoplasmic reticulum stress, leading to insulin resistance and apoptosis.

Keywords:
Endoplasmic reticulum stressLipoapoptosisLipotoxicitySaturated fatty acidSteatosis

More Related Videos

A Model of Experimental Steatosis In Vitro: Hepatocyte Cell Culture in Lipid Overload-Conditioned Medium
08:35

A Model of Experimental Steatosis In Vitro: Hepatocyte Cell Culture in Lipid Overload-Conditioned Medium

Published on: May 18, 2021

6.8K
Author Spotlight: Analysis of Fluorescent-Stained Lipid Droplets with 3D Reconstruction for Hepatic Steatosis Assessment
07:12

Author Spotlight: Analysis of Fluorescent-Stained Lipid Droplets with 3D Reconstruction for Hepatic Steatosis Assessment

Published on: June 2, 2023

6.5K

Related Experiment Videos

Last Updated: May 6, 2026

Author Spotlight: Establishing MASLD Cell Models for Investigating Disease Mechanisms and the Lipid-Lowering Effects of Koumiss
07:03

Author Spotlight: Establishing MASLD Cell Models for Investigating Disease Mechanisms and the Lipid-Lowering Effects of Koumiss

Published on: July 19, 2024

1.9K
A Model of Experimental Steatosis In Vitro: Hepatocyte Cell Culture in Lipid Overload-Conditioned Medium
08:35

A Model of Experimental Steatosis In Vitro: Hepatocyte Cell Culture in Lipid Overload-Conditioned Medium

Published on: May 18, 2021

6.8K
Author Spotlight: Analysis of Fluorescent-Stained Lipid Droplets with 3D Reconstruction for Hepatic Steatosis Assessment
07:12

Author Spotlight: Analysis of Fluorescent-Stained Lipid Droplets with 3D Reconstruction for Hepatic Steatosis Assessment

Published on: June 2, 2023

6.5K

Area of Science:

  • Hepatology
  • Metabolic Syndrome
  • Cellular Biology

Background:

  • Obesity is a major public health concern, contributing to the rising prevalence of non-alcoholic fatty liver disease (NAFLD).
  • NAFLD pathogenesis is increasingly linked to lipotoxicity, involving fatty acid accumulation and altered membrane phospholipid composition, rather than solely triglyceride buildup.
  • Emerging evidence suggests triglyceride accumulation may be protective, while saturated and trans fatty acids are more toxic due to blocked synthesis.

Purpose of the Study:

  • To review the metabolic and redox aspects of lipotoxicity and lipoapoptosis in NAFLD.
  • To highlight the role of endoplasmic reticulum (ER) stress in hepatosteatosis.
  • To discuss the lipotoxic liver injury hypothesis.

Main Methods:

  • Literature review focusing on metabolic and redox pathways.
  • Analysis of studies investigating fatty acid toxicity and cellular responses.
  • Examination of the role of ER stress in NAFLD pathogenesis.

Main Results:

  • Accumulation of specific fatty acids, particularly saturated and trans forms, drives liver injury.
  • Altered membrane phospholipid composition impairs cellular homeostasis and receptor function.
  • Increased cellular saturation induces ER stress, contributing to insulin resistance and apoptosis.

Conclusions:

  • The lipotoxic liver injury hypothesis provides a framework for understanding hepatosteatosis.
  • ER stress and associated signaling pathways are critical mediators of lipotoxicity.
  • Targeting metabolic and redox pathways may offer therapeutic strategies for NAFLD.