The portal hypothesis postulates that the hyper-lipolytic state of intra-abdominal VAT results in the release of non-esterified free fatty acids (46, 48), which through the portal circulation reaches the liver, resulting in increased hepatic glucose production, decreased insulin clearance and hyperinsulinemia, and thus increased very low dense lipoproteins -apolipoprotein B secretion and hypertriglyceridemia (47). The gene discussed is APOB; the disease is hypertriglyceridemia.