To avoid problems associated with abnormal maternal behavior and post-natal lethality in Mest-deficient mice, which would confound the interpretation of MEST function in diet-induced obesity and adipose tissue expansion (ATE), we generated an isogenic (C57BL/6J) mouse model with loxP sites flanking the 3rd exon of Mest to selectively inactivate Mest in a tissue-specific manner. Here, MEST is linked to obesity disorder.