MARK2 and Insulin resistance: Regardless of the relative contributions of these two alternatives, excess hepatic fat appears to be causally linked to hepatic insulin resistance via a number of potential cellular pathways, including deleterious impaired inflammatory signalling, endoplasmic reticulum stress, excess production of reactive oxygen species, mitochondrial dysfunction, accumulation of triglycerides and/or fatty acyl intermediates, and activation of serine-threonine kinases, as recently reviewed [27].