Skip to main content
. Author manuscript; available in PMC: 2013 Dec 1.
Published in final edited form as: Alcohol. 2012 Sep 7;46(8):715–725. doi: 10.1016/j.alcohol.2012.08.004

Table 1.

Comparison of rodent models of alcohol feeding.

Model Species BAC Pathology Advantages/Disadvantages
Lieber-DeCarli oral liquid diet Mice
Rats
100–160 mg/dL Animals develop steatosis, minor inflammatory infiltrates
  • Oral delivery, strict nutritional equality with controls.

  • Activation of Kupffer cells by increased LPS

  • Can be combined with oral gavage to model chronic-binge patterns of alcohol consumption

  • Pathological changes do not progress beyond steatosis, metabolic oxidative stress in the absence of a secondary stress

Ad libitum oral alcohol in drinking water Mice
Rats
50–100 mg/dL Animals develop steatosis, minor inflammatory infiltrates
  • Mimics human consumption and delivery to the gastrointestinal tract.

  • Activation of Kupffer cells by increased LPS

  • Pathological changes do not progress beyond steatosis, metabolic, and oxidative stress in the absence of a secondary stress

Tsukamoto-French intragastic cannulation, enteral feeding model Mice
Rats
As high as 500–600 mg/dL, depending on amount of alcohol. Average achieved is ~200 mg/dL with an oscillating pattern of high and low BAC Animals develop steatosis, inflammatory cell infiltration, necrosis and fibrosis
  • Enteral delivery, maintains nutritional equality with controls

  • Larger dosage of alcohol than oral feeding methods.

  • Progressive pathological changes including fibrosis with activation of Kupffer cells and inflammatory networks

  • Requires surgical expertise for insertion of cannula, which remains in place through duration of treatment.

  • Bypasses effects of alcohol on oral-pharyngeal mucosa and upper GI tract.

  • Contributes to dysbiosis and bacterial overgrowth in the GI tract

  • BAC must be closely monitored to avoid alcohol toxicity

Oral gavage Mice
Rats
Can be in excess of >500 mg/dL Animals develop steatosis and mild inflammatory cell infiltrates
  • Allows for administration of increased dosage of alcohol

  • Models binge drinking, more difficult for chronic consumption

  • Pathological effects when combined with a chronic oral ingestion mimic human pathology

  • Bypasses oral mucosa and upper GI

  • Stressful for animals, with risk of upper GI trauma

  • BAC must be closely monitored to avoid alcohol toxicity

Alcohol preferring rodents (P, iP & NP rats)
(HAP/LAP mice)
40–130 mg/dL can be in excess of 200 mg/dL Animals do not develop cirrhosis
  • Natural oral feeding model, mimics human behavior animals progressively develop HCC in the absence of cirrhosis (rats)

  • Pathological progression from steatosis, oxidative stress, inflammation, necrosis and fibrosis are uncharacterized