Metabolic disruptions in the adipocyte-hepatocyte fatty acid axis as causes of HyperapoB

HyperapoB is the atherogenic dyslipoproteinemia characterized by increased numbers of LDL particles in plasma due to increased secretion of B100 lipoprotein particles by the liver. The lipid phenotype in affected patients is variable but an increased plasma apoB points to the increased LDL particle number. The adipocyte-hepatocyte fatty acid axis refers to the traffic in fatty acids from adipocytes to hepatocytes and back again. Our central thesis is that a reduced rate of adipocyte triglyceride synthesis leads to increased traffic to and fro along this axis. This article outlines the ways in which impaired adipose tissue function leads to increased flux of fatty acids to the liver which leads, in turn, to increased secretion of hepatic B100 particles. The Adipsin-ASP pathway is a newly described biological pathway which appears to play a critical role in regulating adipose tissue triglyceride synthesis. Impaired function of this pathway appears to be the commonest reason for the increased fatty acid traffic in the adipocyte-hepatocyte axis leading to HyperapoB.