Key result
ApoE deficiency increases small intestinal villus height and enhances fat absorption in mice.
Why the study?
Does Apo E deficiency cause morphological changes in the small intestine and enhance fat absorption in mice?
Does Apo E deficiency cause morphological changes in the small intestine and enhance fat absorption in mice?
Hyperplasia of small intestinal villi and enhanced fat absorption are involved in the pathogenesis of hyperlipidemia in apo E deficient mice.
In addition to abnormalities in lipid metabolism, the small intestine, which absorbs fat, plays an important role in the pathogenesis of hyperlipidemia. Using hyperlipidemia/arteriosclerosis models (apo E deficient mice), we measured morphological changes in the small intestinal villi, and investigated fat absorption using a 13C-trioctanoin breath test. In the apo E deficiency groups, the total cholesterol and triglyceride concentrations were higher than the values in the corresponding control groups. The height of the small intestinal villi was increased, showing a histological hyperplastic change. The concentrations of Δ13CO2 were significantly increased, suggesting the enhancement of fat absorption or an increase in the total volume of absorption. In apo E deficient mice, hyperplasia of the small intestinal villi and the enhancement of fat absorption were involved in the pathogenesis of hyperlipidemia. Excessive fat absorption in the small intestine may be one of the etiological factor for hyperlipidemia.
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Noriaki et al. (2006) studied Hyperlipidemia. Apo E deficiency vs. Control mice was evaluated on Morphological changes in small intestinal villi and fat absorption. Apo E deficient mice exhibited increased small intestinal villi height and significantly enhanced fat absorption compared to controls, suggesting a role in hyperlipidemia pathogenesis.
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