ARHGAP21 modulates the secretion of VLDL vesicles in the liver of C57BL/6 mice

ARHGAP21 controls multiple cellular functions, such as migration, proliferation, differentiation and vesicles intracellular traffic. Our ARHGAP21-heterozygous animal model (Het, 50% of the protein expression) treated with the high fat diet (HFD) have higher content of triglycerides in the liver, compared to C57BL/6 animals fed on the same diet. The HFD favored the accumulation of lipids in the Het animal. The liver of our model fed with HFD is more sensitive to insulin than the control animal, which may have led to increased degradation of the proteins involved in the assembly of VLDL, such as MTP, preventing this molecule from being secreted and consequently has became the animal's liver steatotic. In addition, there is a greater gene expression of GLUT2 in het animals, this more glucose reaches the hepatocytes, this overload of glucose may be converted in lipids, and it collaborates with the steatotic state found in this animal.