We hypothesised that the molecular changes triggered in type 2 diabetes might cause phenotypic changes in the lipid fraction of tissues. We compared tissue lipid profiles of inbred lean B6-Bom with those of the obese B6-ob/ob and diabetic BKS-db/db mice and found that genetically diabetic mice significantly accumulate fat (especially monounsaturated fatty acids, MUFA) in non-lipogenic tissues such as the eye (MUFA, 2-fold), skeletal muscle (MUFA, 13-fold) and pancreas (MUFA, 16-fold). In contrast, the B6-ob/ob mice which manifest a milder form of type 2 diabetes use the liver as their predominant lipid depot (MUFA 91-fold increase, as compared to lean mice values). The lipids in the BKS-db/db skeletal muscle and pancreas were also significantly enriched with linoleic acid (LA, (9-fold and 6-fold, respectively); and alpha-linolenic acid (ALA, 8.5-fold and 8-fold, respectively). MUFA, LA and ALA accumulation in the non-lipogenic tissues of BKS-db/db mice was associated with reduced liver stearoyl-CoA desaturase-1 expression.