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 Experiment Videos

Endotoxin, TNF, and IL-1 decrease cholesterol 7 alpha-hydroxylase mRNA levels and activity

K R Feingold1, D K Spady, A S Pollock

  • 1Department of Medicine, University of California, San Francisco 94121, USA.

Journal of Lipid Research
|February 1, 1996
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Kidney tubule health scores and their associations with incident CKD in women living with HIV.

HIV medicine·2021
Same author

Changes in vertebral bone marrow fat and bone mass after gastric bypass surgery: A pilot study.

Bone·2015
Same author

The association of adiposity with kidney function decline among HIV-infected adults: findings from the Fat Redistribution and Metabolic Changes in HIV Infection (FRAM) study.

HIV medicine·2014
Same author

The authors reply.

American journal of epidemiology·2014
Same author

Lessons learned from the design and implementation of myocardial infarction adjudication tailored for HIV clinical cohorts.

American journal of epidemiology·2014
Same author

Urinary biomarkers of kidney injury are associated with all-cause mortality in the Women's Interagency HIV Study (WIHS).

HIV medicine·2013
Same journal

Erratum to 'Stearoyl-CoA desaturase-1 is vital for milk lipid synthesis: Deletion impairs mammary gland and neonatal development' [Journal of Lipid Research 66/12 (2025) 100941].

Journal of lipid research·2026
Same journal

The Metabolic-Immune Axis in MASH: Is the Macrophage Signature the Key to Liver Disease Staging?

Journal of lipid research·2026
Same journal

BK channel deficiency promotes lipolysis via an AKT-independent activation of the cAMP/PKA/HSL pathway.

Journal of lipid research·2026
Same journal

Interleukin-6 stimulates platelet 12-lipoxygenase to drive coagulation in inflammatory arthritis.

Journal of lipid research·2026
Same journal

LIPA regulates myeloid differentiation and is essential for intra-plaque macrophage accumulation during atherogenesis.

Journal of lipid research·2026
Same journal

Hydrolysis and depletion of phosphatidylglycerol at peak murine acute lung injury.

Journal of lipid research·2026
See all related articles

Endotoxin and cytokines rapidly decrease cholesterol 7 alpha-hydroxylase (CAH) mRNA and activity in the liver. This reduction in CAH may contribute to hypercholesterolemia during the acute phase response.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Immunology

Background:

  • Endotoxin (LPS) and cytokines elevate cholesterol synthesis and hepatic lipoprotein secretion, leading to hypercholesterolemia in rodents.
  • Cholesterol 7 alpha-hydroxylase (CAH) is the rate-limiting enzyme for bile acid synthesis, a key pathway for cholesterol elimination.
  • Reduced CAH activity can increase hepatic cholesterol availability for lipoprotein production.

Purpose of the Study:

  • To investigate the effect of LPS, TNF, and IL-1 on hepatic CAH expression and activity.
  • To determine the kinetics and dose-dependency of CAH downregulation by LPS.
  • To assess whether CAH downregulation contributes to LPS-induced hypercholesterolemia.

Main Methods:

  • Administration of LPS, TNF, or IL-1 to Syrian hamsters.

Related Experiment Videos

  • Analysis of CAH mRNA levels in liver tissue via quantitative PCR.
  • Measurement of CAH enzyme activity.
  • Dietary manipulation with colestipol or a cholesterol-enriched diet.

    • Main Results:

    • LPS, TNF, or IL-1 administration caused a significant decrease in hepatic CAH mRNA levels.
    • The decrease in CAH mRNA was rapid, dose-dependent, and occurred even under conditions of increased basal CAH expression or high cholesterol diet.
    • CAH activity was reduced concurrently with mRNA levels, indicating functional downregulation.

    Conclusions:

    • LPS and cytokines rapidly suppress CAH expression and activity in the liver.
    • This suppression of CAH may play a role in the hypercholesterolemia observed during acute inflammatory responses.
    • CAH is identified as a lipid metabolism regulator altered during the acute phase response.