Effect of Nutrients on the Metabolism of Toxic Amyloid Oligomers in Hep G2

High fat high cholesterol diets are linked to Alzheimer’s disease and risk for liver disease in Western communities. Interests in toxic amyloid beta oligomers and liver cell studies with liver steatosis may assist with in the understanding of the risk for neurodegeneration in AD. Human hepatoma Hep G2 cells were treated with either cholesterol/fatty acids or protein solutions and the clearance of amyloid beta oligomers determined. Cholesterol or palmitic acid to liver cells was associated with slower amyloid beta metabolism. Cholesterol reduced the clearance of amyloid beta and palmitic acid increased the secretion of amyloid beta from Hep G2 cells. Hep G2 amyloid beta transport was associated with endosomal and lysosomal lipoprotein transport. Endosomal clearance of amyloid beta was related to lipoprotein contents. Atherogenic lipids and excess lipoprotein prevent liver clearance of toxic amyloid beta oligomers in Hep G2 cells and indicate that high fat high cholesterol diets are closely involved with liver amyloid beta clearance and neurodegeneration in AD.