The APOB48 protein thus produced exclusively by the intestine is processed to synthesize chylomicrons that are responsible for the lipid uptake from the diet. In the liver, the APOB mRNA is translated in the APOB100 protein that is involved in the synthesis of VLDL and LDL. In transgenic rabbits expressing the rbapobec1-shRNA, the level of APOBEC1 gene expression and the level of editing are significantly reduced in the intestine. The ability to synthesize chylomicrons in response to a diet challenge is reduced. The productions of LDL and VLDL are not significantly modified;Shanzhiside-methylester but the production of HDL is modified since HDL is processed from chylomicrons and remnants that are reduced. The lean phenotype is thus consecutive to the reduced lipids uptake by the enterocytes through the low synthesis of chylomicrons after each food challenge. The absence of obese phenotype in transgenic rabbits expressing the human APOBEC1 enzyme in the intestine is amazing. Indeed, we were expecting for a long-term gain of weight in these animals since the human APOBEC1 transgene should have enhanced the level of editing of the APOB mRNA. It has been already published that in the rabbit species, around 90% of the APOB mRNA was edited in the intestine. Accordingly, our results have shown that more than 95% of APOB mRNA were edited. However,Sesamoside in the present study, the expression of the human APOBEC1 transgene was not able to enhance the level of editing, and consequently, animals did not elicit any obese phenotype. One explanation is that the editing was already at its maximum in wild type animals, and that the over-expression of APOBEC1 was inefficient. It has been reported that the editing results from the activity of the APOB mRNA editing complex, a multicomponent protein complex with enzymatic and regulatory activities. Thus, we suggest that the editing was limited by the availability or activity of other components of the editing complex. More surprisingly, in transgenic rabbits expressing the human APOBEC1 gene, the plasma level of triglycerides in the chylomicrons + VLDL fraction was not enhanced after a fat-rich diet for 8 days as it was in wild type rabbits.