Treatment with thiazolidinediones (TZDs) improves glucose homeostasis by increasing
insulin sensitivity, but it also leads to weight gain. Our hypothesis was that, in
individual adipose depots, there is depot specificity for lipid storage and energy
expenditure genes after TZD treatment. After 5 weeks of rosiglitazone treatment on
Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an animal model of type 2 diabetes
mellitus with obesity, and Long-Evans Tokushima Otsuka rats as controls, we measured
changes in lipid storage and energy expenditure gene expression in various adipose
depots, such as mesenteric and nonmesenteric adipose tissues (subcutaneous, epididymal,
and retroperitoneal). Mesenteric fat masses did not change after TZD treatment in
OLETF rats, but nonmesenteric fat masses increased. Messenger RNA expression of lipid
storage genes increased in nonmesenteric fat, but energy expenditure gene expression
increased in mesenteric fat after rosiglitazone treatment. In conclusion, our findings
suggest that TZD treatment may be associated with the depot-specific effects of lipid
storage and energy expenditure genes on fat redistribution in individual adipose tissues
in OLETF rats.