Figure 1.

The complex relationship between T1D, NAFLD, and chronic complications.

Sedentary lifestyle, hyperglycaemia and glycaemic variability, insulin kinetics in the portal circulation, caloric excess, genetic and epigenetic factors and the gut microbiome all potentially contribute to both visceral adipose tissue volume expansion and hepatic and peripheral IR in T1D. These risk factors increase both the prevalence of NAFLD and contribute to increased atherosclerosis and subsequent ischemic heart disease and nephropathy. NAFLD potentially contributes in an independent manner to these complications, increasing the total risk for cardiovascular and renal disease. Furthermore, the relationship between NAFLD and IR is bidirectional, strengthening their cumulative effect. Finally, IR increases the progression towards NASH with significant fibrosis, which in turn further increases the odds for cardiovascular or renal disease.

IR, insulin resistance; NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis; T1D, type 1 diabetes.