CONTEXT: Six-transmembrane protein of prostate 2 (STAMP2) is a counter-regulator 
of inflammation and insulin resistance according to findings in mice. However, 
there have been contradictory reports in humans.
OBJECTIVE: We aimed to explore STAMP2 in association with inflammatory and 
metabolic status of human obesity.
DESIGN, PATIENTS, AND METHODS: STAMP2 gene expression was analyzed in adipose 
tissue samples (171 visceral and 67 sc depots) and during human preadipocyte 
differentiation. Human adipocytes were treated with macrophage-conditioned 
medium, TNF-α, and rosiglitazone.
RESULTS: In visceral adipose tissue, STAMP2 gene expression was significantly 
decreased in obese subjects, mainly in obese subjects with type 2 diabetes. 
STAMP2 gene expression and protein were significantly and inversely associated 
with obesity phenotype measures (body mass index, waist, hip, and fat mass) and 
obesity-associated metabolic disturbances (systolic blood pressure and fasting 
glucose). In addition, STAMP2 gene expression was positively associated with 
lipogenic (FASN, ACC1, SREBP1, THRSP14, TRα, and TRα1), CAV1, IRS1, GLUT4, and 
CD206 gene expression. In sc adipose tissue, STAMP2 gene expression was not 
associated with metabolic parameters. In both fat depots, STAMP2 gene expression 
in stromovascular cells was significantly higher than in mature adipocytes. 
STAMP2 gene expression was significantly increased during the differentiation 
process in parallel to adipogenic genes, being increased in preadipocytes 
derived from lean subjects. Macrophage-conditioned medium (25%) and TNF-α (100 
ng/ml) administration increased whereas rosiglitazone (2 μM) decreased 
significantly STAMP2 gene expression in human differentiated adipocytes.
CONCLUSIONS: Decreased STAMP2 expression (mRNA and protein) might reflect 
visceral adipose dysfunction in subjects with obesity and type 2 diabetes.