Fatty liver is prevalent in apolipoprotein B (apoB)-defective familial hypobetalipoproteinemia (FHBL). Similar to humans, mouse models of FHBL produced by gene targeting (apob+/38.9) manifest low plasma cholesterol and increased hepatic triglycerides (TG) even on a chow diet due to impaired hepatic VLDL-TG secretive capacity. Because apoB truncations shorter than apoB48 are expressed in the intestine, we examined whether FHBL mice may have limited capacity for intestinal dietary TG absorption. In addition, we investigated whether FHBL mice are more susceptible to diet-induced hepatic TG accumulation. Fat absorption capacity was impaired in apoB38.9 mice in a gene dose-dependent manner. Relative fractional fat absorption coefficients for apob+/+, apob+/38.9, and apob38.9/38.9 were 1.00, 0.96, and 0.71, respectively. To raise hepatic TG, we fed high-fat (HF) and low-fat (LF) pellets. Hepatic TG level was observed in rank order: HF > LF > chow. On both LF and HF, liver TG level was higher in the apob+/38.9 than in apob+/+. Hepatic TG secretion remained impaired in the apob +/389 on the HF diet. Thus the FHBL mice are more susceptible to diet-induced fatty liver despite relatively reduced intestinal TG absorption capacity on a HF diet.

Original languageEnglish
Pages (from-to)G146-G152
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Issue number1 52-1
StatePublished - Jul 2005


  • Animal model
  • Dietary fat
  • Familial hypobetalipoproteinemia
  • Fatty liver
  • Intestinal fat absorption


Dive into the research topics of 'Reduced intestinal fat absorptive capacity but enhanced susceptibility to diet-induced fatty liver in mice heterozygous for ApoB38.9 truncation'. Together they form a unique fingerprint.

Cite this