The pre-diabetes and type 2 diabetes spectrum is associated with disordered hormonal regulation of adipose tissue fatty acid metabolism. Resistance to insulin-stimulated dietary fatty acid storage has been described over the past fifteen years and is now clearly documented using a wide array of isotopic tracer methods, including our recent non-invasive positron emission tomography (PET) method able to quantify whole-body organ-specific dietary fatty acid partitioning. Another less well recognized feature of adipose tissues’ metabolic inflexibility is their resistance to catecholamine-stimulated intracellular lipolysis and mobilisation of non-esterified fatty acids (NEFA) to lean organs. Recently, brown adipose tissue (BAT) has been rediscovered in adult humans using 18-fluoro-deoxyglucose PET. Reduced BAT glucose uptake is clearly associated with obesity and type 2 diabetes. However, fatty acids from intracellular triglyceride lipolysis are the main energy source of BAT. Although BAT clearly contributes to cold-induced thermogenesis, its potential for energy dissipation and role in the development of obesity and type 2 diabetes are not elucidated at this time. We found that white adipose tissue NEFA mobilization is linked to total body BAT metabolic capacity. Whether BAT displays metabolic inflexibility with regards to dietary fat utilization and intracellular fatty acid mobilization than white adipose tissues in type 2 diabetes is an intriguing hypothesis under investigation in our laboratory.