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

Ethanol and lipids.

C S Lieber, M Savolainen

    Alcoholism, Clinical and Experimental Research
    |July 1, 1984
    PubMed
    Summary
    This summary is machine-generated.

    Ethanol metabolism in the liver disrupts fat breakdown, promoting fat accumulation and fatty liver. This can lead to hyperlipemia, or high blood lipids, especially in early stages of alcohol abuse.

    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

    Upstream structure of human ADH7 gene and the organ distribution of its expression.

    Biochemical and biophysical research communications·1995
    Same author

    Serum carbohydrate-deficient transferrin: mechanism of increase after chronic alcohol intake.

    Hepatology (Baltimore, Md.)·1995
    Same author

    Medical disorders of alcoholism.

    The New England journal of medicine·1995
    Same author

    First-pass metabolism of alcohol. Absence of diurnal variation and its inhibition by cimetidine after evening meal.

    Digestive diseases and sciences·1995
    Same author

    Significant increase of blood alcohol by cimetidine after repetitive drinking of small alcohol doses.

    Alcoholism, clinical and experimental research·1995
    Same author

    The effect of chronic alcohol administration on cerulein-induced pancreatitis.

    International journal of pancreatology : official journal of the International Association of Pancreatology·1995

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Metabolic Syndrome

    Background:

    • Ethanol is preferentially metabolized by the liver, displacing fatty acids as an energy source.
    • Ethanol oxidation alters the cellular redox state, promoting lipogenesis and fat accumulation in the liver.
    • Chronic alcohol consumption can impair mitochondrial function, further contributing to fatty liver disease.

    Purpose of the Study:

    • To elucidate the complex interactions between ethanol consumption and lipid metabolism.
    • To explain the mechanisms underlying alcohol-induced fatty liver and hyperlipemia.
    • To investigate the impact of ethanol on lipoprotein secretion and blood lipid levels.

    Main Methods:

    • Analysis of ethanol's effects on hepatic energy metabolism and redox state.

    Related Experiment Videos

  • Investigation of ethanol's influence on lipogenesis and acylglycerol formation.
  • Examination of mitochondrial function and endoplasmic reticulum activity in response to chronic ethanol exposure.

    • Main Results:

    • Ethanol consumption leads to fat accumulation in the liver by displacing fat as an energy source and promoting lipogenesis.
    • Chronic alcohol intake results in fatty liver due to depressed mitochondrial oxidative capacity and altered redox state.
    • Ethanol consumption can cause hyperlipemia by stimulating lipoprotein secretion, though this is counteracted by impaired liver secretory capacity.

    Conclusions:

    • The level of blood lipids in alcohol consumers depends on the balance between stimulated lipoprotein secretion and impaired liver function.
    • Early stages of alcohol abuse, with minimal liver damage, are characterized by prevailing hyperlipemia.
    • Severe liver injury from chronic alcohol consumption leads to decreased blood lipids, with implications for cardiovascular health and high-density lipoprotein (HDL) subtypes.