The proposed mechanism for established MS could be that visceral adiposity is associated with impaired glucose tolerance and atherogenic dyslipidaemia, which is a combination of increased triglyceride and reduced HDL levels as well as LDL particles.13,15 As intra-abdominal fat is highly lipolytic and increases fatty acid transport to the liver, a decrease in insulin clearance is inevitable, causing hyperinsulinaemia.17 Furthermore, both visceral obesity and hyperinsulinaemia are associated with increased sympathetic activity, favouring re-absorption of Na+. The gene discussed is INS; the disease is Impaired glucose tolerance.